https://microbewiki.kenyon.edu/index.php?title=Blood_Glucose_Regulation&feed=atom&action=historyBlood Glucose Regulation - Revision history2024-03-28T13:42:25ZRevision history for this page on the wikiMediaWiki 1.39.6https://microbewiki.kenyon.edu/index.php?title=Blood_Glucose_Regulation&diff=119058&oldid=prevTauberb: /* References */2015-12-16T03:01:32Z<p><span dir="auto"><span class="autocomment">References</span></span></p>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[20] Bäckhed F, Ding H, Wang T, Hooper LV, Koh GY, Nagy A, Semenkovich CF, Gordon JI: The gut microbiota as an environmental factor that regulates fat storage. Proc Natl Acad Sci U S A 2004;101:15718–15723</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[20] Bäckhed F, Ding H, Wang T, Hooper LV, Koh GY, Nagy A, Semenkovich CF, Gordon JI: The gut microbiota as an environmental factor that regulates fat storage. Proc Natl Acad Sci U S A 2004;101:15718–15723</div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">[21] Cherrington AD, Diamond MP, Green DR, Williams PE: Evidence for an intra- hepatic contribution to the waning effect of glucagon on glucose production in the conscious dog. Diabetes 31:917–922, 1982</ins></div></td></tr>
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<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">[22] Cherrington AD,(1997) Control of Glucose Uptake and Release by the Liver In Vivo [pdf]. Retrieved from: http://rodrigoborges.hospedagemdesites.ws/principal/pdf/endocrino_07.pdf</ins></div></td></tr>
</table>Tauberbhttps://microbewiki.kenyon.edu/index.php?title=Blood_Glucose_Regulation&diff=119057&oldid=prevTauberb: /* Hormones */2015-12-16T02:57:44Z<p><span dir="auto"><span class="autocomment">Hormones</span></span></p>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> During extreme stimuli the sympathetic nervous system kicks into action. This is colloquially known as the fight or flight response illustrated in figure 4. The brain sends signals throughout the body to increase heart rate, cause bronchial dilation and haptic glucose release. The brain also sends signals to the adrenal glands. Epinephrine is released from the adrenal glands. This hormone is key to the prolonged sympathetic response. [4,10]Epinephrine produces similar results as the initial neuronal signal however it is longer lasting. Epinephrine travels through the blood stream and causes the liver to release glucose thus increasing blood glucose levels in order to be ready for the threat. [4,10]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> During extreme stimuli the sympathetic nervous system kicks into action. This is colloquially known as the fight or flight response illustrated in figure 4. The brain sends signals throughout the body to increase heart rate, cause bronchial dilation and haptic glucose release. The brain also sends signals to the adrenal glands. Epinephrine is released from the adrenal glands. This hormone is key to the prolonged sympathetic response. [4,10]Epinephrine produces similar results as the initial neuronal signal however it is longer lasting. Epinephrine travels through the blood stream and causes the liver to release glucose thus increasing blood glucose levels in order to be ready for the threat. [4,10]</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> The pathway by which this occurs is outlined here. Epinephrine binds to a transmembrane receptor on the liver known as the beta-adrenergic receptor protein. The receptor activates a G protein which then activates. [4,11]The G protein activates by swapping out at GDP for a GTP. Once activated the G protein diffuses along the membrane. The G protein then binds with and activates adenylyl cyclase. Adenylyl cyclase causes ATP to become cyclic AMP (cAMP).The molecule cAMP binds with protein kinase-A which phosporalayts specific proteins. In this step phosphorylase is phosphorylated.[4,11] Phosphorylase then cuts glucogen creating a glucose-1-phosphate. This is further refined into glucose-6-phosphate by phosphoglucomutase. Glucose-6-phosphate can then be used for energy requirements necessary in the sympathetic nervous system response. This allows for more ATP in the muscle and brain.[4,11]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> The pathway by which this occurs is outlined here. Epinephrine binds to a transmembrane receptor on the liver known as the beta-adrenergic receptor protein. The receptor activates a G protein which then activates. [4,11]The G protein activates by swapping out at GDP for a GTP. Once activated the G protein diffuses along the membrane. The G protein then binds with and activates adenylyl cyclase. Adenylyl cyclase causes ATP to become cyclic AMP (cAMP).The molecule cAMP binds with protein kinase-A which phosporalayts specific proteins. In this step phosphorylase is phosphorylated.[4,11] Phosphorylase then cuts glucogen creating a glucose-1-phosphate. This is further refined into glucose-6-phosphate by phosphoglucomutase. Glucose-6-phosphate can then be used for energy requirements necessary in the sympathetic nervous system response. This allows for more ATP in the muscle and brain.[4,11]</div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div> This hormone pathway is reversed when the parasympathetic nervous system takes priority.This system is sometimes referred to as the “rest and digest”.[10,11]</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> This hormone pathway is reversed when the parasympathetic nervous system takes priority.This system is sometimes referred to as the “rest and digest”.[10,11<ins style="font-weight: bold; text-decoration: none;">] An experiment was conducted by Cherrington and colleagues that looked at the effects of blood glucose levels after exogenic epinephrine was inserted. This experiment conducted in conscious dogs looked at hepatic glucose release and showed a 50% increase in hepatic glucose release in response to an amount of epinephrine seen in a moderate stress response.[21,22</ins>]</div></td></tr>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== Diabetes Mellitus ==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>== Diabetes Mellitus ==</div></td></tr>
</table>Tauberbhttps://microbewiki.kenyon.edu/index.php?title=Blood_Glucose_Regulation&diff=119056&oldid=prevTauberb: /* Gut Bacteria */2015-12-16T02:20:18Z<p><span dir="auto"><span class="autocomment">Gut Bacteria</span></span></p>
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 02:20, 16 December 2015</td>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Gut Bacteria==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Gut Bacteria==</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>A connection has been shown between decreased gut bacteria diversity and obesity.[18] Obesity is a risk factor for T2DM. [19] However a causal relationship between gut microbiota and obesity has yet to be proven.[18] In addition obesity doesn't necessarily cause one to have T2DM. In the united states 34% of adults are obese where only 11% have T2DM.[19] It is possible that a change in gut micro flora could cause diabetes but that connection has yet to be shown. An experiment preformed by <del style="font-weight: bold; text-decoration: none;">Gordon </del>and colleagues that could shed light on this showed a germ free mice maintained 40% less body weight compared to control mice. This trend was still seen in germ free mice who received a feeding regiment so that their caloric intake was 29% higher than conventionally raised mice. When these mice received gut microbiota their body fat increase 57% and became "dramatically insulin resistant".[18,20]</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>A connection has been shown between decreased gut bacteria diversity and obesity.[18] Obesity is a risk factor for T2DM. [19] However a causal relationship between gut microbiota and obesity has yet to be proven.[18] In addition obesity doesn't necessarily cause one to have T2DM. In the united states 34% of adults are obese where only 11% have T2DM.[19] It is possible that a change in gut micro flora could cause diabetes but that connection has yet to be shown. An experiment preformed by <ins style="font-weight: bold; text-decoration: none;">Bäckhed </ins>and colleagues that could shed light on this showed a germ free mice maintained 40% less body weight compared to control mice. This trend was still seen in germ free mice who received a feeding regiment so that their caloric intake was 29% higher than conventionally raised mice. When these mice received gut microbiota their body fat increase 57% and became "dramatically insulin resistant".[18,20]</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Conclusion==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Conclusion==</div></td></tr>
</table>Tauberbhttps://microbewiki.kenyon.edu/index.php?title=Blood_Glucose_Regulation&diff=119055&oldid=prevTauberb: /* References */2015-12-16T02:19:17Z<p><span dir="auto"><span class="autocomment">References</span></span></p>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[19]Eckel, R. (2011). Obesity and Type 2 Diabetes: What Can Be Unified and What Needs to Be Individualized?vol. 34 no. 6 1424-1430.doi: 10.2337/dc11-0447</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[19]Eckel, R. (2011). Obesity and Type 2 Diabetes: What Can Be Unified and What Needs to Be Individualized?vol. 34 no. 6 1424-1430.doi: 10.2337/dc11-0447</div></td></tr>
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<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">[20] Bäckhed F, Ding H, Wang T, Hooper LV, Koh GY, Nagy A, Semenkovich CF, Gordon JI: The gut microbiota as an environmental factor that regulates fat storage. Proc Natl Acad Sci U S A 2004;101:15718–15723</ins></div></td></tr>
</table>Tauberbhttps://microbewiki.kenyon.edu/index.php?title=Blood_Glucose_Regulation&diff=119054&oldid=prevTauberb: /* Gut Bacteria */2015-12-16T02:18:28Z<p><span dir="auto"><span class="autocomment">Gut Bacteria</span></span></p>
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 02:18, 16 December 2015</td>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Gut Bacteria==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Gut Bacteria==</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>A connection has been shown between decreased gut bacteria diversity and obesity.[18] Obesity is a risk factor for T2DM. [19] However a causal relationship between gut microbiota and obesity has yet to be proven.[18] In addition obesity doesn't necessarily cause one to have T2DM. In the united states 34% of adults are obese where only 11% have T2DM.[19] It is possible that a change in gut micro flora could cause diabetes but that connection has yet to be shown.</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>A connection has been shown between decreased gut bacteria diversity and obesity.[18] Obesity is a risk factor for T2DM. [19] However a causal relationship between gut microbiota and obesity has yet to be proven.[18] In addition obesity doesn't necessarily cause one to have T2DM. In the united states 34% of adults are obese where only 11% have T2DM.[19] It is possible that a change in gut micro flora could cause diabetes but that connection has yet to be shown. <ins style="font-weight: bold; text-decoration: none;">An experiment preformed by Gordon and colleagues that could shed light on this showed a germ free mice maintained 40% less body weight compared to control mice. This trend was still seen in germ free mice who received a feeding regiment so that their caloric intake was 29% higher than conventionally raised mice. When these mice received gut microbiota their body fat increase 57% and became "dramatically insulin resistant".[18,20]</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Conclusion==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Conclusion==</div></td></tr>
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</table>Tauberbhttps://microbewiki.kenyon.edu/index.php?title=Blood_Glucose_Regulation&diff=118874&oldid=prevTauberb at 01:09, 13 December 20152015-12-13T01:09:00Z<p></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
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<col class="diff-marker" />
<col class="diff-content" />
<tr class="diff-title" lang="en">
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 01:09, 13 December 2015</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l45">Line 45:</td>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> As the liver is key in the release of glucose into the blood stream and issue with it can prevent healthy maintenance of blood glucose levels. With heavy drinking the liver will become fatty reducing it’s effectiveness at releasing energy stores. A disease where inflammation of the liver causes problems with the liver function is called alcoholic hepatitis. The liver can also become hard with heavy drinking due to scare tissue formation this is called fibrosis this is shown in figure 5.</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> As the liver is key in the release of glucose into the blood stream and issue with it can prevent healthy maintenance of blood glucose levels. With heavy drinking the liver will become fatty reducing it’s effectiveness at releasing energy stores. A disease where inflammation of the liver causes problems with the liver function is called alcoholic hepatitis. The liver can also become hard with heavy drinking due to scare tissue formation this is called fibrosis this is shown in figure 5.</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> The pancreas is vital for blood glucose regulation and alcohol can have a significant effect on this organ. The pancreas creates digestive enzymes to metabolize the alcohol and these enzymes destabilize the cell membrane of the pancreatic cells. This leaves the cell liable to auto-digestion.</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> The pancreas is vital for blood glucose regulation and alcohol can have a significant effect on this organ. The pancreas creates digestive enzymes to metabolize the alcohol and these enzymes destabilize the cell membrane of the pancreatic cells. This leaves the cell liable to auto-digestion.</div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">==Gut Bacteria==</ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">A connection has been shown between decreased gut bacteria diversity and obesity.[18] Obesity is a risk factor for T2DM. [19] However a causal relationship between gut microbiota and obesity has yet to be proven.[18] In addition obesity doesn't necessarily cause one to have T2DM. In the united states 34% of adults are obese where only 11% have T2DM.[19] It is possible that a change in gut micro flora could cause diabetes but that connection has yet to be shown.</ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Conclusion==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Conclusion==</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br><br></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br><br></div></td></tr>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[17]Cederbaum, A. I. (2012). ALCOHOL METABOLISM. Clinics in Liver Disease, 16(4), 667–685. http://doi.org/10.1016/j.cld.2012.08.002</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[17]Cederbaum, A. I. (2012). ALCOHOL METABOLISM. Clinics in Liver Disease, 16(4), 667–685. http://doi.org/10.1016/j.cld.2012.08.002</div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">[18] Musso, G.(2010). Obesity, Diabetes, and Gut Microbiota The hygiene hypothesis expanded?, vol. 33 no. 10 2277-2284.doi: 10.2337/dc10-0556</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">[19]Eckel, R. (2011). Obesity and Type 2 Diabetes: What Can Be Unified and What Needs to Be Individualized?vol. 34 no. 6 1424-1430.doi: 10.2337/dc11-0447</ins></div></td></tr>
</table>Tauberbhttps://microbewiki.kenyon.edu/index.php?title=Blood_Glucose_Regulation&diff=118870&oldid=prevTauberb: /* Alcohol effects on glucose regulation */2015-12-12T23:16:19Z<p><span dir="auto"><span class="autocomment">Alcohol effects on glucose regulation</span></span></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 23:16, 12 December 2015</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l43">Line 43:</td>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:liverdamage.jpeg|thumb|300px|left| Effects of Alcohol on Liver[http://charginglife.com/wp-content/uploads/2012/04/liverdamage.jpeg].]]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:liverdamage.jpeg|thumb|300px|left| Effects of Alcohol on Liver[http://charginglife.com/wp-content/uploads/2012/04/liverdamage.jpeg].]]</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> Research also indicates that heavy drinking will cause insulin to become ineffective, resulting in high blood sugar levels. It is unclear if the high blood sugar levels are from heavy drinking alone or are connected to obesity. Further complicating this is a high correlation between heavy drinking and obesity. Also a review of the effects of alcohol indicates that both glycolysis and gluconeogenesis will be inhibited. (cederbaum,2012) </div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> Research also indicates that heavy drinking will cause insulin to become ineffective, resulting in high blood sugar levels. It is unclear if the high blood sugar levels are from heavy drinking alone or are connected to obesity. Further complicating this is a high correlation between heavy drinking and obesity. Also a review of the effects of alcohol indicates that both glycolysis and gluconeogenesis will be inhibited. (cederbaum,2012) </div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div> As the liver is key in the release of glucose into the blood stream and issue with it can prevent healthy maintenance of blood glucose levels. With heavy drinking the liver will become fatty reducing it’s effectiveness at releasing energy stores. A disease where inflammation of the liver causes problems with the liver function is called alcoholic hepatitis. The liver can also become hard with heavy drinking due to scare tissue formation this is called fibrosis.</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> As the liver is key in the release of glucose into the blood stream and issue with it can prevent healthy maintenance of blood glucose levels. With heavy drinking the liver will become fatty reducing it’s effectiveness at releasing energy stores. A disease where inflammation of the liver causes problems with the liver function is called alcoholic hepatitis. The liver can also become hard with heavy drinking due to scare tissue formation this is called fibrosis <ins style="font-weight: bold; text-decoration: none;">this is shown in figure 5</ins>.</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> The pancreas is vital for blood glucose regulation and alcohol can have a significant effect on this organ. The pancreas creates digestive enzymes to metabolize the alcohol and these enzymes destabilize the cell membrane of the pancreatic cells. This leaves the cell liable to auto-digestion.</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> The pancreas is vital for blood glucose regulation and alcohol can have a significant effect on this organ. The pancreas creates digestive enzymes to metabolize the alcohol and these enzymes destabilize the cell membrane of the pancreatic cells. This leaves the cell liable to auto-digestion.</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
</table>Tauberbhttps://microbewiki.kenyon.edu/index.php?title=Blood_Glucose_Regulation&diff=118869&oldid=prevTauberb: /* Alcohol effects on glucose regulation */2015-12-12T23:15:55Z<p><span dir="auto"><span class="autocomment">Alcohol effects on glucose regulation</span></span></p>
<table style="background-color: #fff; color: #202122;" data-mw="interface">
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<col class="diff-content" />
<tr class="diff-title" lang="en">
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 23:15, 12 December 2015</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l41">Line 41:</td>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> In an article published by Gin et al. the findings show no adverse effects on diabetic participants after moderate alcohol consumption. The American Diabetes Association and other medical information outlets concur with this finding, that moderate consumption of alcohol produce no adverse effects. However acute ingestion of alcohol has also been reported to increase insulin secretion, resulting in low blood glucose.[15,17]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> In an article published by Gin et al. the findings show no adverse effects on diabetic participants after moderate alcohol consumption. The American Diabetes Association and other medical information outlets concur with this finding, that moderate consumption of alcohol produce no adverse effects. However acute ingestion of alcohol has also been reported to increase insulin secretion, resulting in low blood glucose.[15,17]</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>[[Image:liverdamage.jpeg|thumb|300px|left|http://charginglife.com/wp-content/uploads/2012/04/liverdamage.jpeg].]]</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>[[Image:liverdamage.jpeg|thumb|300px|left| <ins style="font-weight: bold; text-decoration: none;">Effects of Alcohol on Liver[</ins>http://charginglife.com/wp-content/uploads/2012/04/liverdamage.jpeg].]]</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> Research also indicates that heavy drinking will cause insulin to become ineffective, resulting in high blood sugar levels. It is unclear if the high blood sugar levels are from heavy drinking alone or are connected to obesity. Further complicating this is a high correlation between heavy drinking and obesity. Also a review of the effects of alcohol indicates that both glycolysis and gluconeogenesis will be inhibited. (cederbaum,2012) </div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> Research also indicates that heavy drinking will cause insulin to become ineffective, resulting in high blood sugar levels. It is unclear if the high blood sugar levels are from heavy drinking alone or are connected to obesity. Further complicating this is a high correlation between heavy drinking and obesity. Also a review of the effects of alcohol indicates that both glycolysis and gluconeogenesis will be inhibited. (cederbaum,2012) </div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> As the liver is key in the release of glucose into the blood stream and issue with it can prevent healthy maintenance of blood glucose levels. With heavy drinking the liver will become fatty reducing it’s effectiveness at releasing energy stores. A disease where inflammation of the liver causes problems with the liver function is called alcoholic hepatitis. The liver can also become hard with heavy drinking due to scare tissue formation this is called fibrosis.</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> As the liver is key in the release of glucose into the blood stream and issue with it can prevent healthy maintenance of blood glucose levels. With heavy drinking the liver will become fatty reducing it’s effectiveness at releasing energy stores. A disease where inflammation of the liver causes problems with the liver function is called alcoholic hepatitis. The liver can also become hard with heavy drinking due to scare tissue formation this is called fibrosis.</div></td></tr>
</table>Tauberbhttps://microbewiki.kenyon.edu/index.php?title=Blood_Glucose_Regulation&diff=118868&oldid=prevTauberb: /* Hormones */2015-12-12T23:15:09Z<p><span dir="auto"><span class="autocomment">Hormones</span></span></p>
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 23:15, 12 December 2015</td>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:insulin-receptor-signaling.png|thumb|300px|left| Insulin pathway [http://themedicalbiochemistrypage.org/images/insulin-receptor-signaling.png].]]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:insulin-receptor-signaling.png|thumb|300px|left| Insulin pathway [http://themedicalbiochemistrypage.org/images/insulin-receptor-signaling.png].]]</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>A key regulatory pathway to control blood glucose levels is the hormone insulin. Insulin is released from the beta cells in the islets of Langerhans found in the pancreas. Insulin is released when there is a high concentration of glucose in the blood stream. The beta cells know to release insulin through the fallowing pathway. [2,3]Glucose enters the cell and ATP is produce in the mitochondria through the Krebs cycle and electron transport chain. This increase in ATP causes channels to closes. These channels allow potassium cations to flow into the cell. [2,3,]With these channels closed the inside of the cell becomes more negative causing calcium channels to open allowing calcium cations to flow into the cell. Calcium cation ions flow into the cell due to a concentration and elector chemical gradient that favors the influx of calcium cations. Calcium ions are key in the vesicle excretion processes. A protein on the vesicle called the v-SNARE protein becomes entangled with a t-SNARE protein on the beta cell surface. With calcium facilitating the interaction amongst the SNARE proteins the vesicle is forced to merge with the cell membrane and insulin is excreted into the blood stream.[2,3,4,5]</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>A key regulatory pathway to control blood glucose levels is the hormone insulin. Insulin is released from the beta cells in the islets of Langerhans found in the pancreas. Insulin is released when there is a high concentration of glucose in the blood stream. The beta cells know to release insulin through the fallowing pathway <ins style="font-weight: bold; text-decoration: none;">depicted in figure 2</ins>. [2,3]Glucose enters the cell and ATP is produce in the mitochondria through the Krebs cycle and electron transport chain. This increase in ATP causes channels to closes. These channels allow potassium cations to flow into the cell. [2,3,]With these channels closed the inside of the cell becomes more negative causing calcium channels to open allowing calcium cations to flow into the cell. Calcium cation ions flow into the cell due to a concentration and elector chemical gradient that favors the influx of calcium cations. Calcium ions are key in the vesicle excretion processes. A protein on the vesicle called the v-SNARE protein becomes entangled with a t-SNARE protein on the beta cell surface. With calcium facilitating the interaction amongst the SNARE proteins the vesicle is forced to merge with the cell membrane and insulin is excreted into the blood stream.[2,3,4,5]</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> Insulin travels through the blood stream to muscle, brain or adipose tissue. Once there, the insulin binds to a dimeric transmembrane receptor. This receptor autophosphorylates and causes many downstream pathways relating to glucose regulation, energy storage and DNA transcription. For the glucose regulation pathway the receptor autophosphorylates then causes insulin receptor substrate 1 (IRS-1) to be phosphorated[2,3,4]. IRS-1 then phosphorylates Phosphatidylinositol 3-kinase (PI3K). PI3K cleaves Phosphatidylinositol 4,5-bisphosphate (PIP2) leaving diacyl glycerol (DAG) in the cell membrane and inositol 1,4,5-trisphosphate (IP3) in the cytosol. IP3 travels to the smooth endoplasmic reticulum (SER) and cause calcium channels to open in the SER, releasing cations into the cytosol. DAG activates a kinase named protein kinase C which also opens calcium channels in the SER.[2,3] This ambient increase in calcium facilitates the binding of vesicles to the membrane. These vesicles have Glut4 proteins imbedded in the membrane. Glut4 proteins are channel proteins that allow glucose into the cell. Once these vesicles bind with the cell membrane glucose flows through the Glut4 protein and into the cell, reducing blood glucose levels.[2,3]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> Insulin travels through the blood stream to muscle, brain or adipose tissue. Once there, the insulin binds to a dimeric transmembrane receptor. This receptor autophosphorylates and causes many downstream pathways relating to glucose regulation, energy storage and DNA transcription. For the glucose regulation pathway the receptor autophosphorylates then causes insulin receptor substrate 1 (IRS-1) to be phosphorated[2,3,4]. IRS-1 then phosphorylates Phosphatidylinositol 3-kinase (PI3K). PI3K cleaves Phosphatidylinositol 4,5-bisphosphate (PIP2) leaving diacyl glycerol (DAG) in the cell membrane and inositol 1,4,5-trisphosphate (IP3) in the cytosol. IP3 travels to the smooth endoplasmic reticulum (SER) and cause calcium channels to open in the SER, releasing cations into the cytosol. DAG activates a kinase named protein kinase C which also opens calcium channels in the SER.[2,3] This ambient increase in calcium facilitates the binding of vesicles to the membrane. These vesicles have Glut4 proteins imbedded in the membrane. Glut4 proteins are channel proteins that allow glucose into the cell. Once these vesicles bind with the cell membrane glucose flows through the Glut4 protein and into the cell, reducing blood glucose levels.[2,3]</div></td></tr>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br><b>Glucagon</b></div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br><b>Glucagon</b></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:Glucagon_Activation.png|thumb|300px|right| Glucagon pathway [https://en.wikipedia.org/wiki/Glucagon#/media/File:Glucagon_Activation.png].]]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:Glucagon_Activation.png|thumb|300px|right| Glucagon pathway [https://en.wikipedia.org/wiki/Glucagon#/media/File:Glucagon_Activation.png].]]</div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div> When blood glucose levels are low, glucagon is released which inhibits the break down of glucose, glycolysis and activates the formation of glucose, gluconeogenesis. Gluconeogenesis creates glucose from such molecules as pyruvate, lactate, glycerol, and glucogenic amino acids. Glucagon is released from the alpha cells of the islets of Langerhans in the pancreas.[8] Glucose is brought into the cell through SLC2A1 channel proteins. The glucose is then used to generate ATP. This increase in ATP opens potassium channels unlike in beta cells where they are inhibited. This increase in intercellular potassium causes calcium channels to open which facilitates the binding of vesicles contain glucagon. Glucagon is then released into the blood stream.</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> When blood glucose levels are low, glucagon is released which inhibits the break down of glucose, glycolysis and activates the formation of glucose, gluconeogenesis. Gluconeogenesis creates glucose from such molecules as pyruvate, lactate, glycerol, and glucogenic amino acids. Glucagon is released from the alpha cells of the islets of Langerhans in the pancreas.[8] Glucose is brought into the cell through SLC2A1 channel proteins. The glucose is then used to generate ATP. This increase in ATP opens potassium channels unlike in beta cells where they are inhibited. This increase in intercellular potassium causes calcium channels to open which facilitates the binding of vesicles contain glucagon. Glucagon is then released into the blood stream. <ins style="font-weight: bold; text-decoration: none;">This pathway is shown in figure 3</ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> Glucagon primarily operates on the liver. Once the hormone has made it through the blood stream to the liver it binds to a transmembrane protein called a G protein coupled receptor(GPCR). The associated G protein is phosphorylated with GTP and the alpha unit of the G protein moves to activate adenylate cyclase (AC). AC converts ATP into cyclic AMP (cAMP). [8,9] Cyclic AMP activates protein kinase A (PKA). PKA phosphorylates phosphofructokinase-2 (PFK-2) and fructose bisphosphatase- 2(FBPase-2). Due to the addition of the phosphate PFK-2 becomes less active. This in turn reduces the amount of fructose 2,6-bisphosphate (F-2,6-BP) being produce. High levels of F-2,6-BP cause glycolysis or the break down of glucose.[8,9] So less active PFK-2 decreases the amount of F-2,6-BP. In addition FBPase-2 is activated which breaks downs F-2,6-BP which also decreases the amount of F-2,6-BP. Low levels of F-2,6-BP cause the activation of FBPase-1 which increase gluconeogenesis. In addition there is no activation of PFK-1, which is involved in glycolysis both of these actions increase the amount of blood glucose.[9]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> Glucagon primarily operates on the liver. Once the hormone has made it through the blood stream to the liver it binds to a transmembrane protein called a G protein coupled receptor(GPCR). The associated G protein is phosphorylated with GTP and the alpha unit of the G protein moves to activate adenylate cyclase (AC). AC converts ATP into cyclic AMP (cAMP). [8,9] Cyclic AMP activates protein kinase A (PKA). PKA phosphorylates phosphofructokinase-2 (PFK-2) and fructose bisphosphatase- 2(FBPase-2). Due to the addition of the phosphate PFK-2 becomes less active. This in turn reduces the amount of fructose 2,6-bisphosphate (F-2,6-BP) being produce. High levels of F-2,6-BP cause glycolysis or the break down of glucose.[8,9] So less active PFK-2 decreases the amount of F-2,6-BP. In addition FBPase-2 is activated which breaks downs F-2,6-BP which also decreases the amount of F-2,6-BP. Low levels of F-2,6-BP cause the activation of FBPase-1 which increase gluconeogenesis. In addition there is no activation of PFK-1, which is involved in glycolysis both of these actions increase the amount of blood glucose.[9]</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> </div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> </div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br><b>Epinephrine</b> </div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div><br><b>Epinephrine</b> </div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:autonomic_nervous_system.png |thumb|300px|right| Effects of the Sympathetic Nervous System[http://study.com/cimages/multimages/16/autonomic_nervous_system.png].]]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:autonomic_nervous_system.png |thumb|300px|right| Effects of the Sympathetic Nervous System[http://study.com/cimages/multimages/16/autonomic_nervous_system.png].]]</div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div> During extreme stimuli the sympathetic nervous system kicks into action. This is colloquially known as the fight or flight response. The brain sends signals throughout the body to increase heart rate, cause bronchial dilation and haptic glucose release. The brain also sends signals to the adrenal glands. Epinephrine is released from the adrenal glands. This hormone is key to the prolonged sympathetic response. [4,10]Epinephrine produces similar results as the initial neuronal signal however it is longer lasting. Epinephrine travels through the blood stream and causes the liver to release glucose thus increasing blood glucose levels in order to be ready for the threat. [4,10]</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div> During extreme stimuli the sympathetic nervous system kicks into action. This is colloquially known as the fight or flight response <ins style="font-weight: bold; text-decoration: none;">illustrated in figure 4</ins>. The brain sends signals throughout the body to increase heart rate, cause bronchial dilation and haptic glucose release. The brain also sends signals to the adrenal glands. Epinephrine is released from the adrenal glands. This hormone is key to the prolonged sympathetic response. [4,10]Epinephrine produces similar results as the initial neuronal signal however it is longer lasting. Epinephrine travels through the blood stream and causes the liver to release glucose thus increasing blood glucose levels in order to be ready for the threat. [4,10]</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> The pathway by which this occurs is outlined here. Epinephrine binds to a transmembrane receptor on the liver known as the beta-adrenergic receptor protein. The receptor activates a G protein which then activates. [4,11]The G protein activates by swapping out at GDP for a GTP. Once activated the G protein diffuses along the membrane. The G protein then binds with and activates adenylyl cyclase. Adenylyl cyclase causes ATP to become cyclic AMP (cAMP).The molecule cAMP binds with protein kinase-A which phosporalayts specific proteins. In this step phosphorylase is phosphorylated.[4,11] Phosphorylase then cuts glucogen creating a glucose-1-phosphate. This is further refined into glucose-6-phosphate by phosphoglucomutase. Glucose-6-phosphate can then be used for energy requirements necessary in the sympathetic nervous system response. This allows for more ATP in the muscle and brain.[4,11]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> The pathway by which this occurs is outlined here. Epinephrine binds to a transmembrane receptor on the liver known as the beta-adrenergic receptor protein. The receptor activates a G protein which then activates. [4,11]The G protein activates by swapping out at GDP for a GTP. Once activated the G protein diffuses along the membrane. The G protein then binds with and activates adenylyl cyclase. Adenylyl cyclase causes ATP to become cyclic AMP (cAMP).The molecule cAMP binds with protein kinase-A which phosporalayts specific proteins. In this step phosphorylase is phosphorylated.[4,11] Phosphorylase then cuts glucogen creating a glucose-1-phosphate. This is further refined into glucose-6-phosphate by phosphoglucomutase. Glucose-6-phosphate can then be used for energy requirements necessary in the sympathetic nervous system response. This allows for more ATP in the muscle and brain.[4,11]</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> This hormone pathway is reversed when the parasympathetic nervous system takes priority.This system is sometimes referred to as the “rest and digest”.[10,11]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div> This hormone pathway is reversed when the parasympathetic nervous system takes priority.This system is sometimes referred to as the “rest and digest”.[10,11]</div></td></tr>
</table>Tauberbhttps://microbewiki.kenyon.edu/index.php?title=Blood_Glucose_Regulation&diff=118867&oldid=prevTauberb: /* Introduction */2015-12-12T23:12:29Z<p><span dir="auto"><span class="autocomment">Introduction</span></span></p>
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 23:12, 12 December 2015</td>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Introduction==</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Introduction==</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div><br> Blood glucose regulation involves maintaining blood glucose levels at constant levels in the face of dynamic glucose intake and energy use by the body. <del style="font-weight: bold; text-decoration: none;"> </del>On average this target range is 60-100 mg/dL for an adult although people can be asymptomatic at much more varied levels. In order to maintain this range there are two main hormones that control blood glucose levels: insulin and glucagon. Insulin is released when there are high amounts of glucose in the blood stream. </div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><br> Blood glucose regulation involves maintaining blood glucose levels at constant levels in the face of dynamic glucose intake and energy use by the body. <ins style="font-weight: bold; text-decoration: none;">Glucose, shown in figure 1 is key in the energy intake of humans. </ins>On average this target range is 60-100 mg/dL for an adult although people can be asymptomatic at much more varied levels. In order to maintain this range there are two main hormones that control blood glucose levels: insulin and glucagon. Insulin is released when there are high amounts of glucose in the blood stream. </div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:47dfd3925c5820d42d282aebb1632c23.jpg|thumb|300px|right| Glucose molecule [http://chemwiki.ucdavis.edu/@api/deki/files/42976/47dfd3925c5820d42d282aebb1632c23.jpg?revision=1].]]</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>[[Image:47dfd3925c5820d42d282aebb1632c23.jpg|thumb|300px|right| Glucose molecule [http://chemwiki.ucdavis.edu/@api/deki/files/42976/47dfd3925c5820d42d282aebb1632c23.jpg?revision=1].]]</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>Glucagon is released when there are low levels of glucose in the blood stream. There are other hormones that effect glucose regulation and are mainly controlled by the sympathetic nervous system. Blood glucose regulation is very important to the maintenance of the human body. The brain doesn’t have any energy storage of its own and as a result needs a constant flow of glucose, using about 120 grams of glucose daily or about 60% of total glucose used by the body at resting state. </div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>Glucagon is released when there are low levels of glucose in the blood stream. There are other hormones that effect glucose regulation and are mainly controlled by the sympathetic nervous system. Blood glucose regulation is very important to the maintenance of the human body. The brain doesn’t have any energy storage of its own and as a result needs a constant flow of glucose, using about 120 grams of glucose daily or about 60% of total glucose used by the body at resting state. </div></td></tr>
</table>Tauberb