Research

Hormonal

Intestinal deficiency of Acyl-CoA synthetase 5 (ACSL5) reduces food intake and protects against diet-induced obesity by increasing postprandial secretion of GLP-1 and PYY.

This research suggests that how your body processes dietary fat in the intestine—specifically through the enzyme ACSL5—can influence your hunger hormones (GLP-1 and PYY). When this process is altered, it can lead to increased feelings of fullness and reduced food intake, potentially protecting against weight gain on high-fat diets. While this is a genetic mechanism in mice, it highlights the importance of gut hormones in regulating appetite and energy balance.

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These data indicate that intestinal ACSL5 serves as a critical regulator of energy balance, protecting mice from diet-induced obesity exclusively by increasing satiety and reducing food intake during HFD feeding. The reduction in food intake observed in ACSL5IKO mice is driven, in part, by increased postprandial GLP-1 and PYY secretion.
John D. Griffin et al. · Molecular Metabolism · 2024

Why this rating

High-quality animal study with specific genetic knockout models and mechanistic validation via receptor antagonism.

Source

Intestinal Acyl-CoA synthetase 5 (ACSL5) deficiency potentiates postprandial GLP-1 & PYY secretion, reduces food intake, and protects against diet-induced obesity

John D. Griffin et al. · Molecular Metabolism · 2024

DOI 10.1016/j.molmet.2024.101918

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DOI resolved against Crossref · corpus check 2026-06-10

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