What is it about?
Obesity is the major world’s metabolic disorder affecting more than 1.94 billion people worldwide. Although insulin resistance is commonly observed in obesity, most obese individuals balance the enhanced hormonal demand by increasing insulin secretion, without developing diabetes. Thus, insulin-secreting cells in the pancreas (known as β-cells) undergo “cell adaptation” in an attempt to maintain normoglycaemia despite insulin resistance. The mechanism of β-cell adaptation during the transition from obesity to diabetes is one of the key unanswered questions in our research field. In the recent publication in the journal Diabetes, we reported a new molecular mechanism whereby obesity induces non-canonical activity of the protein STAT3 in the mitochondria of β-cells and its deficiency results in early stages of diabetes development. We used mouse models, stem and primary human cells and cell lines to clarify the mechanism of STAT3 action in glucose control. The present work highlights the potential utility of targeted pharmacological approaches to improve β-cell mitochondrial function in combating the development of diabetes.
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Why is it important?
Most obese individuals balance the enhanced hormonal demand by increasing insulin secretion without developing diabetes. Thus, insulin-secreting cells in the pancreas undergo “adaptation” in an attempt to maintain normoglycaemia despite enhanced insulin demand in obesity. The mechanisms of this process are unclear.
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This page is a summary of: STAT3 Regulates Mitochondrial Gene Expression in Pancreatic β-Cells and Its Deficiency Induces Glucose Intolerance in Obesity, Diabetes, June 2021, American Diabetes Association, DOI: 10.2337/db20-1222.
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