Vol 64, No 1 (2013)
Review paper
Published online: 2013-02-28
Links between growth hormone and aging
Endokrynol Pol 2013;64(1):46-52.
Abstract
Studies in mutant, gene knock-out and transgenic mice have demonstrated that growth hormone (GH) signalling has a major impact on
ageing and longevity. Growth hormone-resistant and GH-deficient animals live much longer than their normal siblings, while transgenic
mice overexpressing GH are short lived. Actions of GH in juvenile animals appear to be particularly important for life extension and
responsible for various phenotypic characteristics of long-lived hypopituitary mutants.
Available evidence indicates that reduced GH signalling is linked to extended longevity by multiple interacting mechanisms including
increased stress resistance, reduced growth, altered profiles of cytokines produced by the adipose tissue, and various metabolic adjustments
such as enhanced insulin sensitivity, increased oxygen consumption (VO2/g) and reduced respiratory quotient. The effects of removing
visceral fat indicate that increased levels of adiponectin and reduced levels of pro-inflammatory cytokines in GH-resistant mice are
responsible for their increased insulin sensitivity. Increased VO2 apparently represents increased energy expenditure for thermogenesis,
because VO2 of mutant and normal mice does not differ at thermoneutral temperature. Recent studies identified GH- and IGF-1-dependent
maintenance of bone marrow populations of very small embryonic-like stem cells (VSELs) as another likely mechanism of delayed ageing
and increased longevity of GH-deficient and GH-resistant animals.
Many of the physiological characteristics of long-lived, GH-related mouse mutants are shared by exceptionally long-lived people and by
individuals genetically predisposed to longevity.
Keywords: growth hormone (GH)calorie restriction (CR)insulin-like growth factor (IGF-1)Ames dwarf micegrowth hormone receptor knockout (GHRKO) mice
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