ArticleAmerican journal of physiology. Endocrinology and metabolism2015
Altered metabolism and resistance to obesity in long-lived mice producing reduced levels of IGF-I.
Article in American journal of physiology. Endocrinology and metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Rapamycin increases oxidative metabolism and enhances metabolic flexibility in human cardiac fibroblasts.GeroScience · 2018Article
- Article
- Impact of Growth Hormone-Related Mutations on Mammalian Aging.Frontiers in genetics · 2018Review
- The somatotropic axis and aging: Benefits of endocrine defects.Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society · 2016Review
- Insulin-like growth factor-1 deficiency and metabolic syndrome.Journal of translational medicine · 2016Review
- Biochemical Genetic Pathways that Modulate Aging in Multiple Species.Cold Spring Harbor perspectives in medicine · 2015Review
- Association between exonic polymorphism (rs629849, Gly1619Arg) of IGF2R gene and obesity in Korean population.Journal of exercise rehabilitation · 2015Article
- Minireview: The Complexities of IGF/Insulin Signaling in Aging: Why Flies and Worms Are Not Humans.Molecular endocrinology (Baltimore, Md.) · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
The extension of lifespan due to reduced insulin-like growth factor 1 (IGF-I) signaling in mice has been proposed to be mediated through alterations in metabolism. Previously, we showed that mice homozygous for an insertion in the Igf1 allele have reduced levels of IGF-I, are smaller, and have an extension of maximum lifespan. Here, we tested whether this specific reduction of IGF-I alters glucose metabolism both on normal rodent chow and in response to high-fat feeding. We found that female IGF-I-deficient mice were lean on a standard rodent diet but paradoxically displayed an insulin-resistant phenotype. However, these mice gained significantly less weight than normal controls when placed on a high-fat diet. In control animals, insulin response was significantly impaired by high-fat feeding, whereas IGF-I-deficient mice showed a much smaller shift in insulin response after high-fat feeding. Gluconeogenesis was also elevated in the IGF-I-deficient mice relative to controls on both normal and high-fat diet. An analysis of metabolism and respiratory quotient over 24 h indicated that the IGF-I-deficient mice preferentially utilized fatty acids as an energy source when placed on a high-fat diet. These results indicate that reduction in the circulating and tissue IGF-I levels can produce a metabolic phenotype in female mice that increases peripheral insulin resistance but renders animals resistant to the deleterious effects of high-fat feeding.
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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.