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Researchers discover molecule’s ability to suppress negative effects of type 2 diabetes, obesity

Key Takeaways

  • Researchers have revealed the mechanisms behind a molecule’s involvement in regulating insulin sensitivity.
  • The findings may serve as the basis for a potential therapeutic target for obesity-related type 2 diabetes.

Macrophages are immune cells that remove dead cells and repair tissues. Adipose tissue macrophages (ATMs) keep the adipose tissue, or body fat, healthy and functioning normally. Prior studies suggest that normal ATM functions help to prevent obesity-related metabolic disease, but the underlying mechanisms are poorly understood.

Researchers from Children’s Hospital of Philadelphia (CHOP) have discovered that a micro RNA called miR-6236 is secreted by ATMs in cases of obesity. (Micro RNA is the name of a family of molecules that helps cells control the kinds and amounts of proteins they make.) Using a preclinical mouse model, the researchers studied the molecule’s function and how it helps balance some of the harmful effects of obesity and type 2 diabetes at a cellular level. Through studies with two preclinical mouse models and a large data set of people at risk for metabolic disease, the researchers also revealed the mechanisms behind the molecule’s involvement in regulating insulin sensitivity. 

The findings, which were published in the journal Nature Communications, may serve as the basis for a potential therapeutic target for obesity-related type 2 diabetes. “Findings like this show that the immune system is central to a healthy metabolism, and hold promise for developing new treatments,” said senior study author David A. Hill, MD, Ph.D. “With this information, a few years from now we could be looking into the development of synthetic micro RNAs, and in the case of miR-6236, there’s a possibility it could be given to patients to improve insulin sensitivity and reduce hyperglycemia,” he added.

Edited by Miriam Kaplan, PhD

Source: Children’s Hospital of Philadelphia, Medical Xpress, June 28, 2024; see source article