Title

Gene expression of key regulators of mitochondrial biogenesis is sex dependent in mice with growth hormone receptor deletion in liver

Authors

Authors

I. Zawada; M. M. Masternak; E. O. List; M. B. Stout; D. E. Berryman; A. Lewinski; J. J. Kopchick; A. Bartke; M. Karbownik-Lewinska;A. Gesing

Comments

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Abbreviated Journal Title

Aging-US

Keywords

mitochondrial biogenesis; gene disruption; growth hormone receptor; knockout mice; tissue-specific gene disruption; sexual dimorphism; KNOCKOUT GHRKO MICE; SKELETAL-MUSCLE; BODY-COMPOSITION; METABOLISM; MOUSE; PARAMETERS; LONGEVITY; ESTRADIOL; PROTEINS; DIET; Cell Biology

Abstract

Mitochondrial biogenesis is an essential process for cell viability. Mice with disruption of the growth hormone receptor (GHR) gene (Ghr gene) in the liver (LiGHRKO), in contrast to long-lived mice with global deletion of the Ghr gene (GHRKO), are characterized by lack of improved insulin sensitivity and severe hepatic steatosis. Tissue-specific disruption of the GHR in liver results in a mouse model with dramatically altered GH/IGF1 axis. We have previously shown increased levels of key regulators of mitochondrial biogenesis in insulin-sensitive GHRKO mice. The aim of the present study is to assess, using real-time PCR, the gene expression of key regulators of mitochondrial biogenesis (Pgc1 alpha, Ampk, Sirt1, Nrf2 and Mfn2) and a marker of mitochondrial activity (CoxIV) in brains, kidneys and livers of male and female LiGHRKO and wild-type (WT) mice. There were significant differences between males and females. In the brain, expression of Pgc1 alpha, Ampk, Sirt1, Nrf2 and Mfn2 was lower in pooled females compared to pooled males. In the kidneys, expression of Ampk and Sirt1 was also lower in female mice. In the liver, no differences between males and females were observed. Sexual dimorphism may play an important role in regulating the biogenesis of mitochondria.

Journal Title

Aging-Us

Volume

7

Issue/Number

3

Publication Date

1-1-2015

Document Type

Article

Language

English

First Page

195

Last Page

204

WOS Identifier

WOS:000352160300008

ISSN

1945-4589

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