Intermittent fasting ameliorates di-(2-ethylhexyl) phthalate-induced precocious puberty in female rats: A study of the hypothalamic-pituitary-gonadal axis.

Di-(2-ethylhexyl) phthalate has been reported to interfere with the development and function of animal reproductive systems. However, hardly any studies provide methods to minimize or prevent the adverse effects of DEHP on reproduction. The energy balance state of mammals is closely related to reproductive activities, and the reproductive axis can regulate reproductive activities according to changes in the body's energy balance state. In this study, the effects of every other day fasting (EODF), as a way of intermittent fasting, on preventing the precocious puberty induced by DEHP in female rats was studied. EODF significantly improved the advancement of vaginal opening age (as the markers of puberty onset) and elevated serum levels of luteinizing hormone and estradiol (detected by ELISA) induced by 5 mg kg-1 DEHP exposure (D5). The mRNA and western blot results showed that the EODF could minimized the increase of gonadotropin-releasing hormone expression induced by DEHP exposure. The administration of DEHP could elevate the levels of kisspeptin protein and the number of kisspeptin-immunoreactive neurons in anteroventral periventricular nucleu, and this increase was diminished considerably by EODF treatment. In contrast, the D5 and D0 groups showed no remarkable difference in the level of Kiss1 expression in arcuate nucleus, whereas the D5 + EODF group had a remarkable decrease in kisspeptin expression as compared with the other two groups. Our results indicated that EODF might inhibit the acceleration of puberty onset induced by DEHP exposure via HPG axis.

Islet ß-cells physiological difference study of old and young mice based on single-cell transcriptomics.

AIMS/INTRODUCTION: Body aging is a universal biological process. With aging, cells undergo a series of physiological changes. The main feature is cell proliferation decline, although the cells still have normal functions. Pancreatic ß-cells are no exception. However, the physiological senescence of ß-cells, and the resulting function and transcriptome changes have rarely attracted attention. The specific senescence phenotype of ß-cells remains unknown. MATERIALS AND METHODS: Pancreatic samples from three female C57BL/6 mice with aged 2.5 months (young) mice and 20 months (old) were digested to a single-cell suspension and analyzed, with 10× Genomics single-cell ribonucleic acid sequencing, ß-cells were determined by biosynthesis analysis, and differences between old and young mice were identified. RESULTS: A total of 47 differential genes with significant and statistical significance were screened in ß-cells (fold change >1.5, P < 0.05). In old mice, 27 genes were upregulated and 20 genes were downregulated. Genes Mt1, Mt2, Pyy, Gcg and Pnlip, and mitochondrial genes mt-Nd1, mt-Nd3, mt-Co1, mt-Co2 and mt-Co3 were found to be involved in cellular senescence. Transcription factors Jund and Fos were important regulators of senescence. CONCLUSIONS: An overall difference was found between the pancreatic ß-cells of old and young mice. Transcription factors facilitate transitions between pancreatic ß-cells. These findings are worthy of deep exploration, and provide new resources and directions for the research of pancreatic aging in mice.