Overexpression of p53 accelerates puberty in high-fat diet-fed mice through Lin28/let-7 system.
Ting ChenCailong ChenHaiying WuXiuli ChenRongrong XieFengyun WangHui SunLinqi ChenPublished in: Experimental biology and medicine (Maywood, N.J.) (2020)
High-fat intake and subsequent obesity are associated with premature onset of puberty, but the exact neuroendocrine mechanisms are still unclear. The transcriptional factor p53 has been predicted to be a central hub of the gene networks controlling the pubertal onset. Besides, p53 also plays crucial roles in metabolism. Here, we explored p53 in the hypothalami of mice fed a high-fat diet (HFD), which showed an up-regulated expression. Besides, we also revealed that overexpressed p53 may accelerate hypothalamo-pituitary-gonadal (HPG) axis activation partially through the c-Myc/Lin28/let-7 system. These results can deepen our understanding of the interaction between metabolic regulation and puberty onset control, and may shed light on the neuroendocrine mechanisms of obesity-related central precocious puberty.
Keyphrases
- high fat diet
- insulin resistance
- high fat diet induced
- adipose tissue
- metabolic syndrome
- skeletal muscle
- transcription factor
- type diabetes
- poor prognosis
- weight gain
- gene expression
- cell proliferation
- copy number
- genome wide
- density functional theory
- dna methylation
- binding protein
- drug induced
- body mass index
- genome wide identification
- heat stress