Obesity is closely associated with numerous adipogenic regulatory factors, including coding and non-coding genes. Long noncoding RNAs (lncRNAs) play a major role in adipogenesis. However, differential expression profiles of lncRNAs in inguinal white adipose tissue (iWAT) between wild-type (WT) and ob/ob mice, as well as their roles in adipogenesis, are not well understood. Here, a total of 2809 lncRNAs were detected in the iWAT of WT and ob/ob mice by RNA-Sequencing (RNA-Seq), including 248 novel lncRNAs. Of them, 46 lncRNAs were expressed differentially in WT and ob/ob mice and were enriched in adipogenesis signaling pathways as determined by KEGG enrichment analysis, including the PI3K/AKT/mTOR and cytokine–cytokine receptor interaction signaling pathways. Furthermore, we focused on one novel lncRNA, which we named lnc-ORA (obesity-related lncRNA), which had a seven-fold higher expression in ob/ob mice than in WT mice. Knockdown of lnc-ORA inhibited preadipocyte proliferation by decreasing the mRNA and protein expression levels of cell cycle markers. Interestingly, lnc-ORA knockdown inhibited adipocyte differentiation by regulating the PI3K/AKT/mTOR signaling pathway. In summary, these findings contribute to a better understanding of adipogenesis in relation to lncRNAs and provide novel potential therapeutic targets for obesity-related metabolic diseases.

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Bisphenol A (BPA), as a widely used plasticizer, is easily absorbed by animals and humans. It has certain toxic effects on various tissues, including liver, heart, kidney, testis, and ovary. The toxic effects of BPA on animal reproduction have aroused widespread concern, but its regulatory mechanism and antidote in female animals estrus cycle remain unclear. In this study, the results displayed that BPA destroyed the normal estrus cycle of mice through decreasing the levels of progesterone and estradiol. Furthermore, BPA significantly increased the levels of oxidative stress, autophagy, and apoptosis in ovaries and granulosa cells. Interestingly, we found that the natural antioxidant resveratrol rescued estrus disorder and impaired estradiol secretion, reduced the abnormal reactive oxygen species accumulation, autophagy, and apoptosis in BPA exposed ovarian tissues. Moreover, transmission electron microscopy showed that resveratrol reduced BPA‐induced autophagic vesicles formation and flow cytometry showed that resveratrol inhibited the increase of apoptotic cells induced by BPA on granulosa cells. Therefore, the supplement of resveratrol could restore BPA‐induced estrus disorder by protecting ovarian granulosa cells. Overall, resveratrol is a potential drug to alleviate BPA‐induced estrous cycle disorders and ovarian damage.

Background Gut health is involved in the nutrition absorption, reproduction and lactation in antenatal, perinatal and early weaned mammals. Recent literatures have demonstrated that melatonin functions in aging, cancer and obesity, but to date, few investigations toward exploring whether melatonin-reprogrammed fecal microbiota transplantation (FMT) and foster care (FC) affect gut health have been performed. Results Here, compared with the control group, melatonin and FMT increased intestinal villus height/crypt depth (V/C), inhibited gut oxidative stress, autophagy and inflammation in antenatal and perinatal rats. Likewise, not only melatonin and FMT, but also FC enhanced intestinal V/C through above parallel ways with decreasing intestinal permeability in early weaned rats. Mechanically, melatonin directly strengthened antioxidation, attenuated autophagy and apoptosis in H2O2-induced IEC6 intestinal epithelial cells. Furthermore, melatonin, FMT and FC reprogrammed intestinal microbiota in which more beneficial microbiota, including Allobaculum, Bifidobacterium and Faecalibaculum produced more metabolic short-chain fatty acids (SCFAs) including acetic acid and butyric acid to protect gut health. Most interestingly, compared with the control group, early weaned rats may get above probiotics via eating or licking the dung of the co-cage rats treated with melatonin in the FC group. Conclusions Overall, melatonin, FMT and FC improved gut health and the potential regulatory mechanism was associated with strengthening antioxidation, suppressing autophagy, inflammatory and apoptosis, as well as producing more SCFAs from reprogrammed gut microbiota. These findings suggest that melatonin, FMT and FC may be novel and effective methods to ameliorate gut health in antenatal, perinatal and weaned mammals.