Objective  Studies have shown that both short-term and long-term cold exposures disturb the biological process. The aim of the present study is to investigate the effects of intermittent cold exposure on proteomic profiles in the hypothalamus and pituitary of female Sprague-Dawley (SD) rats.  Materials and methods  The rats were exposed to -10℃ in a cabin for 4 h per day, and the treatment lasted for 14 days. The comparative label-free LC-MS/MS analysis was performed to investigate the changes of proteomic profiles in the hypothalamus and pituitary. ELISA analysis was used to validate the expression of differential proteins.  Results  22 differential proteins in the hypothalamus and 75 differential proteins in the pituitary were identified by the label-free proteomic analysis. Gene ontology annotation and enrichment analysis indicated that cold exposure disrupted protein phosphorylation, filopodium assembly, intracellular protein transport, peripheral nervous system neuron axonogenesis, spinal cord development, Golgi organization, positive regulation of pseudopodium assembly, and cell-cell adhesion. Three proteins (Cdc42, Ptprs, and Setd7) were down-regulated in the cold exposure group.  Conclusion  The results indicate that intermittent cold exposure alters the proteomic profiles of hypothalamus and pituitary in female rats.

The gut microflora is a combination of all microbes in intestine and their microenvironment, and its change can sensitively reflect the relevant response of the body to external environment and remarkably affect body's metabolism as well. Recent studies have found that cold exposure affects the body's gut microflora, which can lead to changes in the body's metabolism of glucose and lipid. This review summarizes recent research on the effects of cold exposure on gut microbes and metabolism of glucose and lipid, aiming to provide some new ideas on the approaches and measures for the prevention and treatment of diabetes and obesity.

  Background  Long-term exposure to light has emerged as a novel risk factor for metabolic diseases. The whitening of brown adipose tissue (BAT) may play an important role in metabolic disorders caused by long-term continuous light exposure. This study aimed to investigate the morphological and functional alterations in BAT under continuous light conditions and to identify traditional Chinese medicine compounds capable of reversing these changes.  Methods  A metabolic disorder model was established by subjecting mice to continuous light exposure for 5 weeks. During this period, body weight, food intake, and body fat percentage were monitored. Serum levels of triglyceride (TG), total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), and low density lipoprotein cholesterol (LDL-C) were measured to assess lipid metabolism. Histological changes in BAT were examined using H&E staining. The expression of the thermogenic marker uncoupling protein 1 (UCP1) in BAT was determined by RT-qPCR and Western blot to evaluate thermogenic function. RNA sequencing (RNA-seq) was employed to identify differentially expressed genes (DEGs) involved in BAT whitening induced by prolonged continuous light exposure. DEGs were analyzed using the connectivity map (CMap) database to identify potential preventive and therapeutic compounds. The therapeutic efficacy of the selected compounds was subsequently evaluated using the above indicators, and key pathways were validated through western blot analysis.  Results  After 5 weeks of continuous light exposure, mice exhibited increased body fat percentage and serum levels of TG, impaired mitochondrial function, reduced thermogenic capacity, and whitening of BAT. Gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) enrichment analyses indicated that BAT whitening was primarily associated with the adenosine 5'-monophosphate-activated protein kinase (AMPK) signaling pathway, fatty acid metabolism, and circadian rhythm. Ten hub genes identified using Cytoscape were mainly related to AMPK signaling and heat shock proteins. In vivo experiments showed that cordycepin significantly attenuated the increase in body fat percentage caused by prolonged light exposure. This effect was mediated by activation of the AMPK/PGC-1α/UCP1 signaling pathway, which restored the multilocular morphology and thermogenic function of BAT.  Conclusion  Cordycepin mitigates continuous light-induced BAT whitening and metabolic disturbances by activating the AMPK signaling pathway.

  Objective  Nanoparticles (NPs) in haze are potentially hazardous to health, which is more severe in the winter. Brown adipose tissue (BAT) plays important roles in obesity, insulin resistance, and diabetes. Though the toxicology of NPs has been intensively studied, few studies have been reported on the antagonistic effects between Silicon dioxide(SiO₂) NPs and cold exposure in brown adipocytes.  Materials and methods  We evaluated changes by quantitative real-time reverse-transcriptase polymerase chain reaction (qRT-PCR) on metabolism genes, plasticity genes and the inflammatory responses genes in brown adipocytes in vitro.  Results  The expression of adipogenic genes PRDM16, Dio2, PGC-1α and UCP1 was upregulated upon cold exposure (P < 0.05), but downregulated by SiO₂ NPs (P < 0.05). The results demonstrated that there was antagonistic effect between SiO₂ NPs and cold exposure on the plasticity genes and metabolism genes in brown adipocytes, where the main effects of SiO₂ NPs or cold exposure on the plasticity genes and metabolism genes were significant (P < 0.05). Moreover, the levels of interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α were upregulated by SiO₂ NPs or cold exposure (P < 0.05). The factorial analysis indicated that there was also antagonistic effect between SiO₂ NPs and cold exposure on the toxic effects in brown adipocytes, in which the main effects of cold exposure and/or SiO₂ NPs on the toxic effects were significant (P < 0.05).  Conclusion  SiO₂ NPs inhibit the effect of cold exposure on metabolic genes and inflammatory responses genes in brown adipocytes.