Glycerate from intestinal fructose metabolism induces islet cell damage and glucose intolerance

Dietary fructose, especially in the context of a high-fat western diet, has been linked to type 2 diabetes. Although the effect of fructose on liver metabolism has been extensively studied, a significant portion of the fructose is first metabolized in the small intestine. Here, we report that dietary fat enhances intestinal fruc-tose metabolism, which releases glycerate into the blood. Chronic high systemic glycerate levels induce glucose intolerance by slowly damaging pancreatic islet cells and reducing islet sizes. Our findings provide a link between dietary fructose and diabetes that is modulated by dietary fat.

Automated summary

Dietary fructose, especially in the context of a high-fat western diet, has been linked to type 2 diabetes. This study found that dietary fat enhances fructose metabolism in the small intestine, releasing glycerate into the blood. High systemic levels of glycerate cause damage to pancreatic islet cells and reduce islet sizes, leading to glucose intolerance.