MedWire News: Production of the protein adropin is stimulated by fat intake and may be protective against insulin resistance and hepatosteatosis, shows a study in mice.
Adropin is encoded by the energy homeostasis associated gene (Enho), and is expressed in the liver and brain, explain researchers in the journal Cell Metabolism.
Andrew Butler (Louisiana State University, Baton Rouge, USA) and colleagues found that when lean mice (C57BL/6J strain) were fed a high-fat diet they displayed a rapid increase in adropin. However, when the mice returned to a fasting state, adropin levels dropped to around those observed in control mice.
Of note, the researchers found that when mice were fed a high-fat diet for a period of 3 months or more, leading to diet-induced obesity, or were genetically bred to be obese, the expression of Enho in the liver declined.
Butler and team found that when Enho was transgenically overexpressed, or adropin injected, in mice with diet-induced obesity, fatty build up in the liver was reduced and insulin resistance declined. These effects were found to be independent of obesity or food intake.
In addition, adropin was found to regulate expression of the peroxisome proliferator-activated receptor gamma gene in adipose tissue, as well as other hepatic lipogenic genes, suggesting a significant link with lipogenesis and lipid metabolism.
“Adropin may therefore be a factor governing glucose and lipid homeostasis, which protects against hepatosteatosis and hyperinsulinemia associated with obesity,” conclude Butler et al.
They add: “Adropin may form the basis for the development of new therapeutic targets for treating metabolic disorders associated with obesity.”
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