Find out the molecular relationship with obesity and insulin resistance

US scientists say disabling a new molecule discovered in white fat cells has allowed mice to eat foods high in calories without being obese or suffering from inflammation that could lead to the current insulin resistance.

The results of the study, published in the September 28 issue of the journal journal, provide the first known molecular link between heat generation (burning calories to produce heat) and the formation of inflammation in Fat cells, which were once thought to be two controlled processes separately.

Heat production plays an important role in metabolism and maintaining a healthy weight, while inflammation leads to insulin resistance, a marker of diabetes.

The group of scientists led by Mr. Bruce Spiegelman of the Dana-Farber Cancer Institute discovered that the protein TRPV4 , a molecule that acts as a switch, is clearly expressed in white fat cells, which are where store excess calories and accumulate in obese individuals.

In the study, the scientists raised mice without TRPV4 or used a drug to neutralize the protein.

Without TRPV4, white fat cells activate a gene that consumes energy to produce heat, instead of storing excess fat. This process of heat production usually occurs in brown or beige fat cells (often called good fats), mainly in small animals and babies to protect the body in cold weather.

When the calorie-fed mice had no calorie regimen for several weeks, they were not fat while the level of inflammation in adipocytes and insulin resistance decreased.

Mr. Spiegelman emphasized the above finding on the role of TRPV4 that will contribute to finding ways to treat obesity and other metabolic diseases.