Della Guardia Lucio, Wang Ling
Department of Biomedical Sciences for Health, Università degli Studi di Milano, Milan, Italy.
Hubei Key Laboratory of Environmental and Health Effects of Persistent Toxic Substances, School of Environment and Health, Jianghan University, Wuhan, China.
Obes Rev. 2023 Apr;24(4):e13552. doi: 10.1111/obr.13552. Epub 2023 Jan 26.
Dysregulations in energy balance represent a major driver of obesity. Recent evidence suggests that environmental factors also play a pivotal role in inducing weight gain. Chronic exposure to fine particulate matter (PM ) is associated with white adipose tissue (WAT) expansion in animals and higher rates of obesity in humans. This review discusses metabolic adaptions in central and peripheral tissues that promote energy storage and WAT accumulation in PM -exposed animals and humans. Chronic PM exposure produces inflammation and leptin resistance in the hypothalamus, decreasing energy expenditure and increasing food intake. PM promotes the conversion of brown adipocytes toward the white phenotype, resulting in decreased energy expenditure. The development of inflammation in WAT can stimulate adipogenesis and hampers catecholamine-induced lipolysis. PM exposure affects the thyroid, reducing the release of thyroxine and tetraiodothyronine. In addition, PM exposure compromises skeletal muscle fitness by inhibiting Nitric oxide (NO)-dependent microvessel dilation and impairing mitochondrial oxidative capacity, with negative effects on energy expenditure. This evidence suggests that pathological alterations in the hypothalamus, brown adipose tissue, WAT, thyroid, and skeletal muscle can alter energy homeostasis, increasing lipid storage and weight gain in PM -exposed animals and humans. Further studies will enrich this pathophysiological model.
能量平衡失调是肥胖的主要驱动因素。最近的证据表明，环境因素在导致体重增加方面也起着关键作用。长期暴露于细颗粒物（PM）与动物白色脂肪组织（WAT）扩张以及人类更高的肥胖率有关。本综述讨论了在暴露于PM的动物和人类中促进能量储存和WAT积累的中枢和外周组织中的代谢适应。长期暴露于PM会在下丘脑产生炎症和瘦素抵抗，减少能量消耗并增加食物摄入量。PM促进棕色脂肪细胞向白色表型的转变，导致能量消耗减少。WAT中的炎症发展可刺激脂肪生成并阻碍儿茶酚胺诱导的脂肪分解。暴露于PM会影响甲状腺，减少甲状腺素和四碘甲状腺原氨酸的释放。此外，暴露于PM会通过抑制一氧化氮（NO）依赖性微血管扩张和损害线粒体氧化能力来损害骨骼肌健康，对能量消耗产生负面影响。这一证据表明，下丘脑、棕色脂肪组织、WAT、甲状腺和骨骼肌的病理改变可改变能量稳态，增加暴露于PM的动物和人类的脂质储存和体重增加。进一步的研究将丰富这一病理生理模型。
