Thaindian News

Washington, Nov 15 (IANS) A specific human enzyme substantially curbed weight, improved metabolism and efficacy of insulin in mice, a new study shows.

Insulin, produced by the pancreatic gland, helps glucose move from the bloodstream into cells, where it is required for movement, growth and repair. This explains why diabetics who do not make or use insulin can become very weak.

Although the human enzyme IKKbeta proved its effectiveness, it also caused widespread inflammation. The research offered new clues into how obesity, insulin resistance and type 2 diabetes were interconnected, reports journal Endocrinology.

Inflammation is a process by which the body’s white blood cells and chemicals protect us from infection and foreign substances such as bacteria and viruses.

“Turning on this molecule has a very dramatic impact on lipid metabolism,” said Haiyan Xu, assistant professor of medicine at the Warren Alpert Medical School of Brown University in Rhode Island.

Obesity and inflammation are both promoters of insulin resistance, but obesity seems to be the worse one. “Lower body weight is always a beneficial thing for influencing insulin sensitivity,” said Haiyan Xu, who led the study, according to a Brown statement.

In this study, researchers changed the sequence of events for engineered mice by inducing inflammation via IKKbeta in their fatty tissue before they were obese.

The result for metabolism was much more positive than for mice who were left unaltered but were fed the same diets. For both male and female mice, the ones who were altered still put on weight but significantly more slowly.

All the mice started at the same weight. After about 22 weeks on a high-fat diet, however, altered male mice weighed less than 38 grams while unaltered male mice weighed more than 45 grams.