Green tea catechin EGCG could prevent obesity-related precocious puberty through NKB/NK3R signaling pathway

Qiuyun Gu; Xiaodi Wang; Luyao Xie; Xinyuan Yao; Linxi Qian; Zhiping Yu; Xiuhua Shen

doi:10.1016/j.jnutbio.2022.109085

Green tea catechin EGCG could prevent obesity-related precocious puberty through NKB/NK3R signaling pathway

J Nutr Biochem. 2022 Oct:108:109085. doi: 10.1016/j.jnutbio.2022.109085. Epub 2022 Jun 10.

Authors

Qiuyun Gu¹, Xiaodi Wang², Luyao Xie², Xinyuan Yao², Linxi Qian³, Zhiping Yu⁴, Xiuhua Shen⁵

Affiliations

¹ Department of Nutrition, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Department of Nutrition, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
² Department of Nutrition, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
³ Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
⁴ Department of Nutrition and Dietetics, Brooks College of Health, University of North Florida, Jacksonville, Florida, USA.
⁵ Department of Nutrition, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Shanghai Key Laboratory of Pediatric Gastroenterology and Nutrition, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China; Department of Nutrition, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: srachel@126.com.

PMID: 35691596
DOI: 10.1016/j.jnutbio.2022.109085

Abstract

This study aimed to explore the potential regulatory pathways of (-)-epigallocatechin-3-gallate (EGCG) in preventing obesity-related precocious puberty. A retrospective analysis on the impact of EGCG on puberty onset in obese girls was conducted on plasma samples collected from a human randomized controlled trial. In the trial, participants consumed EGCG capsules for 12 weeks. In the animal experiment, rats were divided into four groups: normal diet control (NC) group, high-fat diet (HFD) group, NC+EGCG group, and HFD+EGCG group. Blood samples were collected on postnatal days 27, 33, and 36 to detect sexual development indicators. The hypothalamic expressions of kisspeptin/Kiss1R and neurokinin B (NKB)/NK3R signaling were measured by RT-qPCR and Western blot assay. The ovary NKB protein expression was assessed by immunohistochemical assays. Serum NKB level in the EGCG group was lower than the placebo group by 0.599 ng/mL [β=-0.599, 95% CI: (-1.005, -0.193)], at the end of intervention and after adjusting for confounders (clinical study). In the animal experiment, EGCG intervention could significantly delay the vaginal opening (VO) time of rats fed with HFD. On day 33, EGCG intervention could significantly reduce serum NKB, luteinizing hormone (LH) levels, ovarian NKB protein expression, and endometrial thickness of HFD-fed rats, while EGCG intervention could remarkably increase mRNA and protein expression of NKB/NK3R. EGCG could prevent obesity-related precocious puberty through NKB/NK3R signaling pathway, which may provide a novel insight into the role of EGCG in preventing precocious puberty in obese girls.

Keywords: EGCG; Obesity; Precocious puberty; Sex hormones; VO.

Publication types

Randomized Controlled Trial
Research Support, Non-U.S. Gov't

MeSH terms

Animals
Camellia sinensis* / chemistry
Catechin* / administration & dosage
Catechin* / analogs & derivatives
Catechin* / pharmacology
Female
Humans
Neurokinin B / genetics
Neurokinin B / metabolism
Obesity* / complications
Puberty, Precocious* / etiology
Puberty, Precocious* / prevention & control
Rats
Retrospective Studies
Signal Transduction

Substances

Neurokinin B
Catechin
epigallocatechin gallate