4.5 Article

Cold-induced adaptive thermogenesis is impaired by exposure of Asian sand dust in mice

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JOURNAL OF THERMAL BIOLOGY
卷 116, 期 -, 页码 -

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PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jtherbio.2023.103675

关键词

Asian sand dust; Thermogenesis; brown adipose tissue; Ucp1; Obesity; Cold exposure

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Desertification and desert sandstorms caused by global warming increase the risks to human health, especially in relation to Asian sand dust (ASD) exposure which has been found to be associated with higher mortality and hospitalizations due to respiratory diseases. This study shows that ASD administration in mice leads to accumulation of lipid droplets in brown adipose tissues (BAT) and reduced expression of thermogenic genes, impairing cold-induced adaptive thermogenesis. Chronic administration of ASD in mice on a high-fat diet also resulted in unexplained weight loss, indicating potential lethality in obese mice. However, lung inflammation induced by ASD was not exacerbated in mice lacking uncoupling protein 1, which is involved in thermogenesis. Overall, ASD exposure impairs cold-induced adaptive thermogenic responses in mice and increases mortality risk in obese mice.
Desertification and desert sandstorms caused by the worsening global warming pose increasing risks to human health. In particular, Asian sand dust (ASD) exposure has been related to an increase in mortality and hospital admissions for respiratory diseases. In this study, we investigated the effects of ASD on metabolic tissues in comparison to diesel particulate matter (DPM) that is known to cause adverse health effects. We found that larger lipid droplets were accumulated in the brown adipose tissues (BAT) of ASD-administered but not DPMadministered mice. Thermogenic gene expression was decreased in these mice as well. When ASDadministered mice were exposed to the cold, they failed to maintain their body temperature, suggesting that the ASD administration had led to impairments in cold-induced adaptive thermogenesis. However, impaired thermogenesis was not observed in DPM-administered mice. Furthermore, mice fed a high-fat diet that were chronically administered ASD demonstrated unexplained weight loss, indicating that chronic administration of ASD could be lethal in obese mice. We further identified that ASD-induced lung inflammation was not exacerbated in uncoupling protein 1 knockout mice, whose thermogenic capacity is impaired. Collectively, ASD exposure can impair cold-induced adaptive thermogenic responses in mice and increase the risk of mortality in obese mice.

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