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| gainingmuscle mass, microsoftexcel body fat calculator, computer language, lanier, how to lose weight, environment, sourcesfat diet, grabber, food processing, human body composition, sportline, askthe dietitian, mortality, cellular, extension, inkjet, donkeys, nuclear weapons, missile defense, pig weaning, | How does cramp this destructive cycle begin? To understand GPR40's role, Prof. Michael Walker and students Nir Rubins and Reut cramp Bartoov-Shifman of the Weizmann Institute's Biological Chemistry Department teamed up with Prof. Helena Edlund and post-doctoral fellow Dr. Per Steneberg of the University of Umea. Together, they developed two types of lab mice with modified GPR40 activity. In the first, the scientists used a technique known as gene knock-out to prevent production of the GPR40 receptor. The second type had overactive GPR40 genes creating a surfeit of fat-signaling receptors that cramp tricked the beta cells into sensing high fatty acid levels, even on a normal diet. |
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| If sugar remains in the bloodstream, the insulin-producing beta cells in the pancreas compensate by stepping up production. Eventually this leads to beta cell exhaustion, reduced insulin output and the appearance of full-blown cellular diabetes. Elevated fat in the bloodstream appears to accelerate both stages of the disease; but exactly how does this happen? The culprit may be cellular a receptor known as GPR40 found on the outer surface of pancreatic beta cells. GPR40 was recently discovered to respond to cellular fatty acids, alerting beta cells to their presence in the bloodstream. Beta cells were known to be attuned to changes in blood glucose levels, responding to after-meal glucose surges with a sharp increase in insulin production. But when fat is present in addition to sugar, the GPR40 receptor causes even greater insulin output. Frequent overstimulation of the beta cells may be tied to persistently elevated insulin levels, hastening the onset of the disease. |
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