FuturePundit has the scoop on some interesting research reported in Cell Metabolism

A new study in the January 7th issue of Cell Metabolism, a Cell Press publication, helps to explain why obese people and animals fail to respond to leptin, a hormone produced by fat that signals the brain to stop eating. What's more, they show that two FDA-approved drugs might restore leptin sensitivity, offering a novel treatment for obesity.

" Most importantly, our study is the first success in sensitizing obese mice on a high-fat diet to leptin," said Umut Ozcan of Harvard Medical School. "If it works in humans, it could treat obesity."

When leptin was first discovered some 13 years ago, it led to great excitement in the field, Ozcan said. Studies showed that leptin administered to obese mice that lacked the hormone lost weight. The buzz over leptin's potential as an obesity therapy soon waned, however, because obese animals and people don't respond to the hormone. Efforts to find drugs that act as leptin sensitizers over the years have also failed.

A part of cells known as the endoplasmic reticulum (ER) is involved in many cellular processes including protein manufacturing, lipid and carbohydrate synthesis, and other functions. Stress in the ER appears to play a role in a metabolic disorder linked to obesity. These researchers decided that perhaps ER stress played a role in reduced response of the brain's hypothalamus to leptin.

Leptin looked exciting, at first, but it didn't seem to pan out. Now we know why.

So, you want to cut your appetite? Stop stressing the endoplasmic reticulum. Gosh, if only it were as easy as it sounds!

As a side benefit, cutting the ER stress might be crucial to fighting aging as well. See how all this stuff works together?