Researchers at the UT Southwestern Medical Center have discovered how the “starvation hormone" adiponectin works, which ultimately could lead to new treatments for a conditions such as cancer, diabetes, heart disease and obesity.
Researchers used models of inducible cell suicide in both pancreatic beta cells, which produce insulin, and cardiomyocytes, which are specific muscle cells located in a part of the heart known as the myocardium, to determine how the single hormone could exert different influences.
“Until now, there wasn’t really an obvious connection between all these different phenomena," said senior author Dr. Philipp Scherer. “This paper shows that the common theme among all these different activities relies on adiponectin’s interaction with a specific subset of lipids known as ceramides."
Ceramides are known to promote cell suicide, or apoptosis. High levels of ceramides have been shown to promote diabetes by sabotaging signaling pathways induced by insulin and killing beta cells. When the researchers introduced adiponectin into cells, they found that the hormone triggers the conversion of ceramides from a destructive force into one that helps cells survive and inhibits cell death.
Adiponectin controls sensitivity to insulin and is known to play an integral role in metabolism and obesity. Prior research has shown that when adiponectin levels are high, the body stores excess fat in adipocytes, or fat cells, to protect against possible starvation during lean times. These fat deposits lie primarily in the subcutaneous tissue.
However, adiponectin levels decline as a person accumulates more fat. Once adiponectin levels start dropping, the body begins storing fat in dangerous places such as the heart, liver and muscle tissues where it can cause inflammation and pave the way for heart disease. Researchers think adiponectin levels could be a good predictor of whether someone is at risk of developing diabetes, heart disease or cancer.
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