Frontiers in nutrition · 2026
Research on the mechanism of cow milk protein dietary intervention in ameliorating systemic chronic inflammation in type 2 diabetes by disrupting the ROS-M1 macrophage axis.
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Zhang Fumei, Bai Lin, Yang Heqiang, Yang Jianrong, Sun Zhuxin, Wei Jia, Qiao Zilin, Wei Yumei, Song Fei, Tian Xiaojing, Hu Xiaoxia
Аннотация
INTRODUCTION: Recent studies suggest that type 2 diabetes mellitus (T2DM) is characterized by a systemic, low-grade chronic inflammatory state. Although cow milk protein (CMP) has been shown to alleviate this inflammation, its underlying mechanisms remain unclear.
METHODS: Therefore, we investigated how CMP mitigates systemic chronic inflammation in T2DM using both in vitro digestion and mouse models.
RESULTS: The in vitro digestion model demonstrated that CMP, with its low degree of hydrolysis, exhibits significant anti-α-amylase and antioxidant activities. In the in vivo study, CMP markedly reduced fasting blood glucose (FBG) and reversed diabetes-related body weight loss. CMP intervention significantly decreased oxidative stress markers, including malondialdehyde (MDA) and reactive oxygen species (ROS), while enhancing the activity of the antioxidant enzyme glutathione peroxidase (GSH-Px). Moreover, CMP suppressed macrophage polarization toward the M1 phenotype and reduced the levels of pro-inflammatory cytokines. Finally, CMP administration ameliorated lipid infiltration in the liver and intestine, mitigated pancreatic islet atrophy, and concurrently alleviated renal pathologies such as glomerular hypertrophy, glycation, and fibrosis.
DISCUSSION: In conclusion, CMP ameliorates systemic chronic inflammation in T2DM by disrupting the ROS-M1 macrophage vicious cycle.
METHODS: Therefore, we investigated how CMP mitigates systemic chronic inflammation in T2DM using both in vitro digestion and mouse models.
RESULTS: The in vitro digestion model demonstrated that CMP, with its low degree of hydrolysis, exhibits significant anti-α-amylase and antioxidant activities. In the in vivo study, CMP markedly reduced fasting blood glucose (FBG) and reversed diabetes-related body weight loss. CMP intervention significantly decreased oxidative stress markers, including malondialdehyde (MDA) and reactive oxygen species (ROS), while enhancing the activity of the antioxidant enzyme glutathione peroxidase (GSH-Px). Moreover, CMP suppressed macrophage polarization toward the M1 phenotype and reduced the levels of pro-inflammatory cytokines. Finally, CMP administration ameliorated lipid infiltration in the liver and intestine, mitigated pancreatic islet atrophy, and concurrently alleviated renal pathologies such as glomerular hypertrophy, glycation, and fibrosis.
DISCUSSION: In conclusion, CMP ameliorates systemic chronic inflammation in T2DM by disrupting the ROS-M1 macrophage vicious cycle.