Fine particulate matter induces adipose tissue expansion and weight gain: Pathophysiology

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 (PM2.5) 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 PM2.5-exposed animals and humans.Chronic PM2.5 exposure produces inflammation and leptin resistance in the hypothalamus, decreasing energy expenditure and increasing food intake. PM2.5 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. PM2.5 exposure affects the thyroid, reducing the release of thyroxine and tetraiodothyronine. In addition, PM2.5 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 PM2.5-exposed animals and humans. Further studies will enrich this pathophysiological model.

Automated summary

Dysregulations in energy balance and environmental factors, such as chronic exposure to PM2.5, contribute to obesity. PM2.5 exposure leads to inflammation, leptin resistance, and metabolic alterations in the hypothalamus, adipose tissue, thyroid, and skeletal muscle, resulting in increased energy storage and weight gain. Further studies are needed to better understand this pathophysiological model.