all Gokhan Hotamisligil stories

New class of hormone from “healthy fat cells” benefits body metabolism in mice

404132862 — Thu, 18 Sep 2008 12:12:20 -0400

Scientists at the Harvard School of Public Health (HSPH) have identified in mice a newly discovered class of hormones -- lipokines. In tomorrow's issue of the journal Cell they report that lipokine is a molecule in mice that helps stop, or even reverses obesity-related conditions such as insulin resistance and “fatty liver.”

Lipokines are hormones made from lipids, or fats. All other known hormones – chemical signals secreted into the blood that regulate distant cells and organs – are steroid or protein-based.

Key gene discovered for obesity and diabetes

70652986 — Mon, 26 Mar 2007 05:26:14 -0400

Obesity is closely associated with insulin resistance and is one of the leading risk factors for type 2 diabetes. Both affect more than 50 percent of the U.S. population. Little has been known about the molecular mechanisms linking these two metabolic diseases. Both are associated with a wide range of inflammatory molecular activity in fatty tissue. This activity puts into motion the JNK genes that interfere with insulin sensitivity. Type 2 diabetes usually occurs after age 40. People with this type of diabetes do not produce adequate amounts of insulin for the needs of the body and/or cannot use insulin effectively. To test the role of JNK in decreasing insulin sensitivity in a variety of obesity models, a research team bred mice lacking either form of the gene JNK1 or JNK2 and mice possessing the JNK genes. Weight gain rose the sharpest over an eight-week span for the mice on a high-fat diet but particularly for those with the JNK genes. In studying total body fat composition, JNK-deficient mice had significantly decreased total body fat accumulation in comparison. The research findings appeared in the Nov. 21, 2002 issue of the journal Nature.

Researchers identify genes that control development of fat tissues

70652986 — Mon, 26 Mar 2007 05:06:37 -0400

Until now, no one knew the specific trigger that controls the extent to which cells called preadipocytes turn into fat cells. Harvard researchers have identified the genes GATA-2 and GATA-3 as the molecular gatekeepers of that transition. When the genes are defective or missing, preadipocytes change into fat cells and, conversely, when the genes are expressed, preadipocytes remain fixed in a pre-fat stasis and do not accumulate lipids. "If a gene is controlling this critical gate, then one can control the fat tissue in two ways," said Gökhan Hotamisligil, associate professor in the Division of Biological Sciences and Department of Nutrition, who led the study. "Theoretically, one can enhance or diminish the formation of fat cells depending on how one manipulates the genes." Qiang Tong, research fellow in nutrition in the Department of Nutrition, served as first author of the paper.