For people with type 2 diabetes, the problem of insulin resistance means there is plenty of insulin but the body does not respond to it effectively. While most people associate this resistance with sugar levels in the blood, diabetes is also a problem with excess fat, especially too much fat inside skeletal muscle, which leads to the insulin resistance. If the level of fat in muscles can be reduced then, theoretically, insulin resistance can be prevented, surmise investigators.

A new link between high levels of certain amino acids and type 2 diabetes was found using mouse and human muscle and blood samples to evaluate the mechanisms that lead to insulin resistance. The findings of this study appear in Nature Medicine.

The team found that a byproduct compound of breakdown of branched chain amino acids, called 3-HIB, is secreted from muscle cells and activates cells in the vascular wall to transport more fat into skeletal muscle tissue. This leads to fat accumulation in the muscle, in turn leading to insulin resistance in mice. Conversely, inhibiting the synthesis of 3-HIB in muscle cells blocked the uptake of fat in muscle.

"In this study we showed a new mechanism to explain how 3-HIB, by regulating the transport of fatty acids in and out of muscle, links the breakdown of branched-chain amino acids with fatty acid accumulation, showing how increased amino acid flux can cause diabetes," author said.

While most of this research was conducted using mouse cells, the team also found that 3-HIB, the byproduct molecule, was elevated in people with type 2 diabetes. Because of this, researchers say that more studies are needed to fully examine the nature of this mechanism among people with type 2 diabetes.

http://www.uphs.upenn.edu/news/News_Releases/2016/03/arany/