Using a non-radioactive in situ hybridization detection method, we found that fasting up-regulated leptin receptor mRNA expression in the brain of C57 Bl/6 lean (+/+) but not obese (ob/ob) mice. After the lean mice were fasted for 24 h, increased leptin receptor mRNA expression was found in the arcuate and ventromedial hypothalamic nuclei, medial habenular nucleus and dentate gyrus of hippocampal formation. There was only a minor increase in mRNA expression of leptin receptor in the hippocampus proper while the piriform cortex remained unchanged. However, after the obese mice were fasted for 24 h, no detectable changes of leptin receptor mRNA expression could be found. These results indicated that leptin receptor gene expression was influenced by nutritional status. Further, genetically obese mice showed an inability to respond to nutritional change, probably due to the fact that obese mice lack leptin.
Objective This study examined the effects of miR‐122–enriched exosomes on the expression of vitamin D3 receptor (VDR) and sterol regulatory element‐binding transcription factor 1 (SREBF1) and their roles during adipogenesis. Methods The roles of miR‐122, SREBF1, and VDR were investigated during adipogenesis. The relationships between VDR and miR‐122 or SREBF1 were assessed by dual‐luciferase reporter and chromatin immunoprecipitation assays. The potential role of miR‐122/VDR/SREBF1 was evaluated in high‐fat diet‐induced obese male mice. Results High levels of miR‐122 were found only in adipose tissue‐derived exosomes (Exo‐AT) and Exo‐AT–treated cells. Overexpression of miR‐122 promoted adipogenesis, and inhibition of miR‐122 prevented adipogenesis by regulating VDR, SREBF1, peroxisome proliferator‐activated receptor gamma, lipoprotein lipase, and adiponectin. Knockdown of Srebf1 or overexpression of VDR could inhibit adipogenesis. However, exosomal miR‐122 could reverse their inhibitory effects. The dual‐luciferase reporter assay and chromatin immunoprecipitation assays confirmed that VDR was a direct target of miR‐122. It could bind to the BS1 region of the SREBF1 promoter and inhibit SREBF1 expression. Moreover, miR‐122 inhibition could alleviate obesity in high‐fat diet‐induced obese male mice, possibly through upregulating the VDR/SREBF1 axis. Conclusion MiR‐122–enriched Exo‐AT promoted adipogenesis by regulating the VDR/SREBF1 axis.
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