DOI: 10.57760/sciencedb.j00217.11592
title: Research progress on exercise-induced macrophage trained immune tolerance in improving insulin resistance
title: 运动诱导巨噬细胞训练免疫耐受改善胰岛素抵抗的研究进展

description: A high-fat diet can induce insulin resistance (IR) by triggering trained immunity (TI) in macrophages. By modulating the tolerance of innate immune cells to TI and blocking the pathological cycle between IR and TI, it is possible to alleviate chronic inflammation caused by metabolism abnormalities secondary to IR, providing a new targeted intervention point for preventing and treating insulin resistance. Numerous studies have shown that exercise can alter macrophage metabolism, thereby changing their polarization phenotype to improve overall metabolism and alleviate chronic inflammation. Exercise promotes metabolic reprogramming in macrophages through oxidative phosphorylation and mitochondrial fatty acid oxidation, which induces trained immunity tolerance and drives macrophages toward an anti-inflammatory M2 phenotype. At the same time, cellular energy metabolism is enhanced, glucose uptake and mitochondrial function are improved, and reactive oxygen species clearance is increased. These changes collectively promote the conversion of immune cells to an anti-inflammatory phenotype and inhibit pro-inflammatory expression, thereby reducing systemic inflammation and improving IR. However, the specific signaling mechanisms by which exercise drives metabolic reprogramming to induce immune tolerance in macrophages still need further clarification, and related experiments are required for validation. This article aims to explore the mechanisms and related signaling pathways by which exercise induces immune tolerance in macrophages through metabolic reprogramming to improve IR, with the goal of providing new perspectives for the prevention and treatment of metabolic diseases.
description: A high-fat diet can induce insulin resistance (IR) by triggering trained immunity (TI) in macrophages. By modulating the tolerance of innate immune cells to TI and blocking the pathological cycle between IR and TI, it is possible to alleviate chronic inflammation caused by metabolism abnormalities secondary to IR, providing a new targeted intervention point for preventing and treating insulin resistance. Numerous studies have shown that exercise can alter macrophage metabolism, thereby changing their polarization phenotype to improve overall metabolism and alleviate chronic inflammation. Exercise promotes metabolic reprogramming in macrophages through oxidative phosphorylation and mitochondrial fatty acid oxidation, which induces trained immunity tolerance and drives macrophages toward an anti-inflammatory M2 phenotype. At the same time, cellular energy metabolism is enhanced, glucose uptake and mitochondrial function are improved, and reactive oxygen species clearance is increased. These changes collectively promote the conversion of immune cells to an anti-inflammatory phenotype and inhibit pro-inflammatory expression, thereby reducing systemic inflammation and improving IR. However, the specific signaling mechanisms by which exercise drives metabolic reprogramming to induce immune tolerance in macrophages still need further clarification, and related experiments are required for validation. This article aims to explore the mechanisms and related signaling pathways by which exercise induces immune tolerance in macrophages through metabolic reprogramming to improve IR, with the goal of providing new perspectives for the prevention and treatment of metabolic diseases.