Expression of key regulators of mitochondrial biogenesis in Growth Hormone Receptor Knockout (GHRKO) mice is enhanced but is not further improved by other potential life-extending interventions

Adam Gesing, Michal M. Masternak, Feiya Wang, Anna Maria Joseph, Christiaan Leeuwenburgh, Reyhan Westbrook, Andrzej Lewinski, Malgorzata Karbownik-Lewinska, Andrzej Bartke

Research output: Contribution to journalArticle


Mitochondrial biogenesis is essential for cell viability. Growth hormone receptor knockout (GHRKO), calorie restriction, and surgical visceral fat removal constitute experimental interventions to delay aging and increase life span. We examined the expression of known regulators of mitochondriogenesis: peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α), adenosine monophosphate (AMP)-activated protein kinase (AMPK), sirtuin-1 (SIRT-1) and sirtuin-3 (SIRT-3), endothelial nitric oxide synthase (eNOS), nuclear respiratory factor-1, mitochondrial transcription factor A (TFAM), and mitofusin-2 (MFN-2) in the skeletal muscles and hearts of control and calorie-restricted female GHRKO mice and in the kidneys of male GHRKOs after visceral fat removal or sham surgery. Expression of PGC-1α in skeletal muscles, AMPK, SIRT-1, SIRT-3, eNOS, and MFN-2 in the heart and PGC-1α, AMPK, SIRT-3, eNOS, and MFN-2 in kidneys was increased in GHRKO mice but was not affected by calorie restriction or visceral fat removal. GHRKO mice have increased expression of key regulators of mitochondriogenesis, which is not improved further by calorie restriction or visceral fat removal.

Original languageEnglish (US)
Pages (from-to)1062-1076
Number of pages15
JournalJournals of Gerontology - Series A Biological Sciences and Medical Sciences
Volume66 A
Issue number10
Publication statusPublished - Oct 1 2011
Externally publishedYes



  • Calorie restriction
  • Gene expression
  • GHRKO mice
  • Mitochondrial biogenesis
  • Visceral fat removal

ASJC Scopus subject areas

  • Aging
  • Geriatrics and Gerontology
  • Medicine(all)

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