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Liver response affects obesity and diabetes

A study published in the online edition of the journal Nature, found a sensor in the liver (LXR) activated by glucose that controls the body's metabolism of cholesterol and fat.

Scientists fed synthetic LXR to mice eating a diet of mostly simple sugars. They discovered that the mice metabolized glucose more effectively and that activation suppressed new production of glucose in the liver. That prompted the scientists to study glucose levels as the LXR activating mechanism in the liver. By controlling glucose sensing and fat synthesis by LXR, scientists may explain and correct why low-fat, high-carbohydrate diets can lead to an elevated level of triglycerides in the blood. LXR can sense surplus glucose, induce fatty acid synthesis, and prompt the liver's export of triglycerides into the bloodstream rather than being stored as fat.

LXR could resolve the problem of hyperglycemia and atherosclerosis by binding to glucose and cholesterol buildup in the body. LXR induced regression of atherosclerosis, the clogging, narrowing, and hardening of the body's large arteries and blood vessels that can lead to stroke, heart attack, and eye and kidney problems. Contrary to conventional wisdom, this experiment led to the discovery that glucose binds directly to LXR, representing the first signaling pathway of this kind.

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