Kou Guangning, Yao Shuai, Ullah Amin, Fang Shuhao, Guo Erni, Bo Yacong
Centre for Nutritional Ecology and Centre for Sport Nutrition and Health, Zhengzhou University, Zhengzhou 450001, China; Department of Nutrition and Food Hygiene, School of Public Health, Zhengzhou University, Zhengzhou 450001, China.
Centre for Nutritional Ecology and Centre for Sport Nutrition and Health, Zhengzhou University, Zhengzhou 450001, China.
J Hazard Mater. 2025 Jul 15;492:138225. doi: 10.1016/j.jhazmat.2025.138225. Epub 2025 Apr 8.
Microplastics (MPs) are pervasive in the environment and food. The potential health hazards of this emerging pollutant have raised significant concerns in recent years. However, the underlying mechanism by which MPs have any impact on brown and beige adipocytes in the context of obesity is yet to be investigated.
The C57BL/6 J mice were randomly assigned to the HFD and HFD+MPs group for 12 weeks of exposure to explore the differences in brown and beige adipocyte function. The gut microbiota analysis, fecal microbiota transplantation and metabolomic profiling were carried out to further determine its potential mechanism.
The present work demonstrated that high-fat diet mice accumulate lipids and have reduced energy expenditure after three months of oral administration of MPs. In addition to escalating intestinal dysbiosis, exposing HFD mice to MPs induces thermogenic dysfunction in inguinal white adipose tissue and brown adipose tissue. Following the fecal microbiota transplantation, the accumulation of lipids and dysfunction in energy expenditure within the microbiota of recipient mice further elucidated the inhibitory effect of MPs.
Our results suggest that MPs induced the thermogenic dysfunction of BAT and iWAT by affecting gut microbiota composition. The present study highlights the mechanisms by which MPs produce thermogenic dysfunction in BAT and iWAT and disruption in the gastrointestinal microbiota.
微塑料在环境和食物中广泛存在。近年来，这种新兴污染物的潜在健康危害引发了人们的高度关注。然而，在肥胖背景下微塑料对棕色和米色脂肪细胞产生影响的潜在机制尚待研究。
将C57BL/6 J小鼠随机分为高脂饮食组和高脂饮食+微塑料组，进行为期12周的暴露实验，以探究棕色和米色脂肪细胞功能的差异。进行肠道微生物群分析、粪便微生物群移植和代谢组学分析，以进一步确定其潜在机制。
目前的研究表明，高脂饮食小鼠在口服微塑料三个月后会积累脂质并减少能量消耗。除了加剧肠道菌群失调外，将高脂饮食小鼠暴露于微塑料中会导致腹股沟白色脂肪组织和棕色脂肪组织的产热功能障碍。粪便微生物群移植后，受体小鼠微生物群中脂质的积累和能量消耗的功能障碍进一步阐明了微塑料的抑制作用。
我们的结果表明，微塑料通过影响肠道微生物群组成诱导棕色脂肪组织和腹股沟白色脂肪组织的产热功能障碍。本研究突出了微塑料在棕色脂肪组织和腹股沟白色脂肪组织中产生产热功能障碍以及破坏胃肠道微生物群的机制。
