ArticleEndocrinology2015
Growth hormone receptor antagonist transgenic mice are protected from hyperinsulinemia and glucose intolerance despite obesity when placed on a HF diet.
Article in Endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 24 citations in OpenAlex.
- Growth Hormone Receptor Antagonism Extends Lifespan.Aging cell · 2026Article
- PICK1-Deficient Mice Maintain Their Glucose Tolerance During Diet-Induced Obesity.Journal of the Endocrine Society · 2023Article
- Short-Term Growth Hormone Administration Mediates Hepatic Fatty Acid Uptake and De Novo Lipogenesis Gene Expression in Obese Rats.Biomedicines · 2023Article
- Mice with gene alterations in the GH and IGF family.Pituitary · 2022Review
- Review
- Mouse models of growth hormone insensitivity.Reviews in endocrine & metabolic disorders · 2021Review
- The effects of growth hormone on adipose tissue: old observations, new mechanisms.Nature reviews. Endocrinology · 2020Review
- Hormesis in Health and Chronic Diseases.Trends in endocrinology and metabolism: TEM · 2019Review
- Adult-Onset Hepatocyte GH Resistance Promotes NASH in Male Mice, Without Severe Systemic Metabolic Dysfunction.Endocrinology · 2018Article
- Hepatic lipid metabolism and non-alcoholic fatty liver disease in aging.Molecular and cellular endocrinology · 2017Review
- Growth Hormone's Effect on Adipose Tissue: Quality versus Quantity.International journal of molecular sciences · 2017Review
- Growth Hormone Control of Hepatic Lipid Metabolism.Diabetes · 2016Article
- Glucose and Palmitate Differentially Regulate PFKFB3/iPFK2 and Inflammatory Responses in Mouse Intestinal Epithelial Cells.Scientific reports · 2016Article
- Hepatic PPARγ Is Not Essential for the Rapid Development of Steatosis After Loss of Hepatic GH Signaling, in Adult Male Mice.Endocrinology · 2016Article
- 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
- Article
- Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Reduced GH levels have been associated with improved glucose metabolism and increased longevity despite obesity in multiple mouse lines. However, one mouse line, the GH receptor antagonist (GHA) transgenic mouse, defies this trend because it has reduced GH action and increased adiposity, but glucose metabolism and life span are similar to controls. Slight differences in glucose metabolism and adiposity profiles can become exaggerated on a high-fat (HF) diet. Thus, in this study, male and female GHA and wild-type (WT) mice in a C57BL/6 background were placed on HF and low-fat (LF) diets for 11 weeks, starting at 10 weeks of age, to assess how GHA mice respond to additional metabolic stress of HF feeding. On a HF diet, all mice showed significant weight gain, although GHA gained weight more dramatically than WT mice, with males gaining more than females. Most of this weight gain was due to an increase in fat mass with WT mice increasing primarily in the white adipose tissue perigonadal depots, whereas GHA mice gained in both the sc and perigonadal white adipose tissue regions. Notably, GHA mice were somewhat protected from detrimental glucose metabolism changes on a HF diet because they had only modest increases in serum glucose levels, remained glucose tolerant, and did not develop hyperinsulinemia. Sex differences were observed in many measures with males reacting more dramatically to both a reduction in GH action and HF diet. In conclusion, our findings show that GHA mice, which are already obese, are susceptible to further adipose tissue expansion with HF feeding while remaining resilient to alterations in glucose homeostasis.
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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.