ArticleExperimental gerontology2014
Growth hormone abolishes beneficial effects of calorie restriction in long-lived Ames dwarf mice.
Article in Experimental gerontology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Impact of visceral adipose tissue on longevity and metabolic health: a comparative study of gene expression in perirenal and epididymal fat of Ames dwarf mice.GeroScience · 2024Article
- Unveiling ceramide dynamics: Shedding light on healthy aging in growth hormone-releasing hormone knockout mice.Aging cell · 2024Article
- Dietary restriction in senolysis and prevention and treatment of disease.Critical reviews in food science and nutrition · 2024Review
- microRNA-449a reduces growth hormone-stimulated senescent cell burden through PI3K-mTOR signaling.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Rapamycin treatment early in life reprograms aging: hyperfunction theory and clinical practice.Aging · 2022Article
- Molecular mechanisms of dietary restriction promoting health and longevity.Nature reviews. Molecular cell biology · 2022Review
- Decline in biological resilience as key manifestation of aging: Potential mechanisms and role in health and longevity.Mechanisms of ageing and development · 2021Review
- The Role of Ames Dwarfism and Calorie Restriction on Gut Microbiota.The journals of gerontology. Series A, Biological sciences and medical sciences · 2020Article
- Review
- Dietary and Endocrine Regulation of Endogenous Hydrogen Sulfide Production: Implications for Longevity.Antioxidants & redox signaling · 2018Article
- Ovarian aging and the activation of the primordial follicle reserve in the long-lived Ames dwarf and the short-lived bGH transgenic mice.Molecular and cellular endocrinology · 2017Article
- A Long-lived Mouse Lacking Both Growth Hormone and Growth Hormone Receptor: A New Animal Model for Aging Studies.The journals of gerontology. Series A, Biological sciences and medical sciences · 2017Article
- Growth hormone reverses dyslipidemia in adult offspring after maternal undernutrition.Scientific reports · 2017Article
- Hypothalamic-Pituitary Axis Regulates Hydrogen Sulfide Production.Cell metabolism · 2017Article
- Article
- Circadian clocks govern calorie restriction-mediated life span extension through BMAL1- and IGF-1-dependent mechanisms.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Reduced growth hormone signaling and methionine restriction: interventions that improve metabolic health and extend life span.Annals of the New York Academy of Sciences · 2016Review
- When Anti-Aging Studies Meet Cancer Chemoprevention: Can Anti-Aging Agent Kill Two Birds with One Blow?Current pharmacology reports · 2015Article
- The adipokine leptin mediates muscle- and liver-derived IGF-1 in aged mice.Experimental gerontology · 2015Article
- The somatotropic axis and longevity in mice.American journal of physiology. Endocrinology and metabolism · 2015Review
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 3 countries.
Funding
Abstract
Disruption of the growth hormone (GH) axis promotes longevity and delays aging. In contrast, GH over-expression may lead to accelerated aging and shorter life. Calorie restriction (CR) improves insulin sensitivity and may extend lifespan. Long-lived Ames dwarf (df/df) mice have additional extension of longevity when subjected to 30% CR. The aim of the study was to assess effects of CR or GH replacement therapy separately and as a combined (CR+GH) treatment in GH-deficient df/df and normal mice, on selected metabolic parameters (e.g., insulin, glucose, cholesterol), insulin signaling components (e.g., insulin receptor [IR] β-subunit, phosphorylated form of IR [IR pY1158], protein kinase C ζ/λ [p-PKCζ/λ] and mTOR [p-mTOR]), transcription factor p-CREB, and components of the mitogen-activated protein kinase (MAPK) signaling (p-ERK1/2, p-p38), responsible for cell proliferation, differentiation and survival. CR decreased plasma levels of insulin, glucose, cholesterol and leptin, and increased hepatic IR β-subunit and IR pY1158 levels as well as IR, IRS-1 and GLUT-2 gene expression compared to ad libitum feeding, showing a significant beneficial diet intervention effect. Moreover, hepatic protein levels of p-PKCζ/λ, p-mTOR and p-p38 decreased, and p-CREB increased in CR mice. On the contrary, GH increased levels of glucose, cholesterol and leptin in plasma, and p-mTOR or p-p38 in livers, and decreased plasma adiponectin and hepatic IR β-subunit compared to saline treatment. There were no GH effects on adiponectin in N mice. Moreover, GH replacement therapy did not affect IR, IRS-1 and GLUT-2 gene expression. GH treatment abolishes the beneficial effects of CR; it may suggest an important role of GH-IGF1 axis in mediating the CR action. Suppressed somatotrophic signaling seems to predominate over GH replacement therapy in the context of the examined parameters and signaling pathways.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.