Mechanistic insights into EGCG's preventive effects on obesity-induced precocious puberty through multi-omics...

Area of Science:

• Endocrinology
• Microbiology
• Neuroscience

Background:

• Obesity is linked to precocious puberty, a condition with unclear underlying mechanisms.
• Epigallocatechin gallate (EGCG), a compound from green tea, shows potential in addressing this issue.
• Understanding EGCG's impact on obesity-induced precocious puberty is crucial for developing effective interventions.

Purpose of the Study:

• To investigate the mechanisms by which EGCG affects obesity-induced precocious puberty in female mice.
• To evaluate the influence of EGCG on body weight, puberty onset, sex hormone levels, gut microbiota, metabolites, and hypothalamic gene expression.
• To explore the role of the gut-brain axis in mediating EGCG's effects.

Main Methods:

• Female mice were divided into control, EGCG-treated, high-fat diet (HFD), and HFD with EGCG treatment groups.
• Measurements included body weight, vaginal opening time, serum sex hormones, gut microbiota (16S rRNA sequencing), fecal metabolites (metabolomics), and hypothalamic transcriptome (RNA sequencing).

Main Results:

• EGCG treatment mitigated weight gain and delayed vaginal opening in mice on an HFD.
• EGCG reduced serum estradiol levels and the number of mature ovarian follicles.
• EGCG partially reversed HFD-induced gut dysbiosis, increasing beneficial bacteria like Akkermansia, and altered tryptophan metabolism and hypothalamic gene expression.

Conclusions:

• EGCG effectively prevents obesity-induced precocious puberty.
• EGCG exerts its effects by modulating the gut microbiota, altering metabolic pathways, and regulating hypothalamic gene expression.
• These findings highlight the gut-brain axis as a key mediator of EGCG's therapeutic actions.