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17β-estradiol improves hepatic mitochondrial biogenesis and function through PGC1B.

Bel M Galmés-Pascual1,2, Antonia Nadal-Casellas1, Marco Bauza-Thorbrügge1,2

  • 1Departament de Biologia Fonamental i Ciències de la SalutGrup Metabolisme Energètic i Nutrició, Institut Universitari d'Investigació en Ciències de la Salut (IUNICS), Universitat de les Illes Balears, Palma de Mallorca, Illes Balears, Spain.

The Journal of Endocrinology
|November 26, 2016
PubMed
Summary

Estrogen (E2) enhances liver mitochondrial function and biogenesis, counteracting negative effects of estrogen deficiency. This protective role is mediated by PGC1B, highlighting its therapeutic potential for liver mitochondrial disorders.

Keywords:
17β-estradiolHepG2 cellsPGC1livermitochondrial biogenesis and functionovariectomy

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Area of Science:

  • * Endocrinology
  • * Cellular Biology
  • * Metabolism

Background:

  • * Sexual dimorphism impacts mitochondrial biogenesis and function across rat tissues.
  • * Female rats exhibit larger, more functional mitochondria.
  • * Peroxisome proliferator-activated receptor gamma coactivator 1 (PGC1) family members regulate mitochondrial processes, with limited understanding of hepatic PGC1A and PGC1B roles.

Purpose of the Study:

  • * To investigate the role of 17β-estradiol (E2) in liver mitochondrial biogenesis and function.
  • * To determine the contribution of hepatic PGC1A and PGC1B in mediating E2's effects.
  • * To elucidate the protective mechanisms of E2 in hepatocytes.

Main Methods:

  • * Ovariectomized (OVX) rat model with and without E2 treatment.
  • * In vitro studies using HepG2 hepatocytes.
  • * Gene knockdown experiments using small interfering RNA (siRNA) targeting PGC1A and PGC1B.

Main Results:

  • * Estrogen deficiency in OVX rats impaired mitochondrial biogenesis, function, and lipid metabolism, increasing oxidative stress.
  • * E2 treatment counteracted these negative effects.
  • * In HepG2 cells, E2 enhanced mitochondrial biogenesis and function; these effects were independent of PGC1A but dependent on PGC1B.
  • * Knockdown of PGC1B significantly impaired E2's beneficial effects on hepatocyte mitochondria.

Conclusions:

  • * 17β-estradiol (E2) exerts widespread protective effects in hepatocytes by enhancing mitochondrial content, oxidative capacity, and reducing lipid accumulation and oxidative stress.
  • * Hepatic PGC1B acts as a novel mediator of E2's effects on mitochondrial biogenesis and function.
  • * PGC1B activation presents a potential therapeutic strategy for managing hepatic mitochondrial disorders.