The journal Diabetes Care reports obese adults who lost a substantial amount of weight through lifestyle modification and dieting regained less weight when they took the diet drug Xenical, This approach was also associated with a reduced occurrence of type 2 diabetes.

Xenical burns fat while you are eating by inhibiting the absorption of dietary fat from your food. Studies have shown that the drug promotes more weight loss than lifestyle modification alone. The study examined the effectst of Xenical in preventing weight regain in 383 obese adults who had lost an average of 31.7 pounds (14.4 kg) on an 8-week protein-rich, very-low-energy diet. The 309 participants who lost 5% or more of their bodyweight then received lifestyle counseling for 3 years while taking either Xenical or a placebo pill daily. Both groups regained some weight. Xenical patients regained an average of 10 pounds, while placebo patients put back an average of 15 pounds.

Most importantly, during the 3-year study period only 8 of 153 in the Xenical group developed type 2 diabetes compared with 17 of 156 in the placebo group. That's remarkable. Twice as many people were diagnosed with type 2 diabetes, in addition to regaining one and a half times the weight. As an aside (and not to be a whistleblower) but one of the warnings on the label says the drug should not be taken for more than 2 years. Just an FYI.

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.