Oat β-Glucan Supplementation Alleviates Dietary AGE-Induced Hepatic Lipid Metabolism Disorder through Transcriptional Regulation and a Proposed Physical Barrier Effect on Intestinal AGE Absorption.

Dietary advanced glycation end-products (AGEs) contribute to insulin resistance and hepatic steatosis. This study investigated whether oat β-glucan (OBG) could alleviate AGE-induced metabolic dysfunction in Leprdb/db mice. Mice were fed a high-AGE (HA) diet, with OBG administered either by coingestion (HOS) or alternate-day intake (HOA). OBG supplementation reduced weight gain, hyperinsulinemia, and hepatic lipid accumulation without affecting food intake. Histology showed attenuated lipid deposition in the liver and kidney, with HOS exhibiting stronger improvement. Transcriptomics and gene set enrichment analysis revealed that OBG coingestion enhanced glycolysis, the TCA cycle, oxidative phosphorylation, and fatty acid oxidation, while downregulating steatosis-related genes. Western blot validated protein-level changes in key lipid regulators. These findings indicate that OBG protects against AGE-induced metabolic disorder mainly through transcriptional reprogramming of hepatic glucose and lipid metabolism. The superior efficacy of coingested OBG may be related to its potential physical barrier effect on intestinal AGE absorption, which needs to be further verified by direct experimental evidence.