Growth hormone and aging
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Growth hormone and aging Andrzej Bartke 1 Accepted: 11 September 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Growth hormone (GH) actions impact growth, metabolism, and body composition and have been associated with aging and longevity. Lack of GH results in slower growth, delayed maturation, and reduced body size and can lead to delayed aging, increased healthspan, and a remarkable extension of longevity. Adult body size, which is a GH-dependent trait, has a negative association with longevity in several mammalian species. Mechanistic links between GH and aging include evolutionarily conserved insulin/insulin-like growth factors and mechanistic target of rapamycin signaling pathways in accordance with long-suspected trade-offs between anabolic/growth processes and longevity. Height and the rate and regulation of GH secretion have been related to human aging, but longevity is not extended in humans with syndromes of GH deficiency or resistance. However, the risk of age-related chronic disease is reduced in individuals affected by these syndromes and various indices of increased healthspan have been reported.
Keywords GH excess . GH resistance . Growth hormone . Human aging . Lifespan . Healthspan . Mice
1 Introduction There is considerable evidence that actions of pituitary growth hormone (GH) have an important impact on the process of aging in mammals. However, there are quantitative differences in this role of GH in different species. In this article, we will review the effects of GH on aging in laboratory populations of mice (Mus musculus), the mechanisms believed to link GH signaling to aging and longevity in this species, and the relationship of GH and GH-dependent traits to age-related disease, healthspan and lifespan in other mammalian species, including humans. We will close with a discussion of tradeoffs between growth, reproduction, and aging. We will highlight the remarkable evolutionary conservation of signaling mechanisms that underlie these trade-offs and determine the trajectory of aging in organisms ranging from unicellular yeast and simple microscopic worms to insects and vertebrates.
* Andrzej Bartke [email protected] 1
Southern Illinois University School of Medicine, 801 N. Rutledge, P.O. Box 19628, Springfield, IL 62794-9628, USA
2 GH signaling impacts aging in laboratory mice Long survival of mice with hereditary dwarfism was described almost 50 years ago in a study of age-related osteoarthritis [1]. Studies conducted in the ‘90s provided evidence that two types of dwarf mice with deficiency of GH, prolactin, and thyroid-stimulating hormone (TSH) live much longer than their normal siblings [2, 3]. Altered endocrine function in these mutants is due to the loss of function of the Pituitary-1 (Pit-1) or Prophet of Pit-1 (Prop1) transcription factors and the resulting defects in the differentiation of the corresponding cell lineages in the anterior pituitary [4, 5]. Extended longevity of Ames dwarf (Prop1df) mice was believed to be due primarily to GH de
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