ArticleEndocrinology2011
Elevated GH/IGF-I, due to somatotrope-specific loss of both IGF-I and insulin receptors, alters glucose homeostasis and insulin sensitivity in a diet-dependent manner.
Article in Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 43 citations in OpenAlex.
- Low Liver-Derived IGF-1 Drives the Alterations in Growth Hormone Secretion in Food-Restricted Male Mice.Endocrinology · 2025Article
- Liver injury severity determines skeletal deterioration: a shared pathophysiological axis between MASLD and osteoarthritis.GeroScience · 2025Article
- Central and peripheral regulation of the GH/IGF-1 axis: GHRH and beyond.Reviews in endocrine & metabolic disorders · 2025Review
- GH-Releasing Hormone Neurons Regulate the Hypothalamic-Pituitary-Somatotropic Axis via Short-Loop Negative Feedback.Endocrinology · 2025Article
- Characterization and Regulation of the Neonatal Growth Hormone Surge.Endocrinology · 2024Article
- Modifications of the GH Axis Reveal Unique Sexually Dimorphic Liver Signatures forJournal of the Endocrine Society · 2024Article
- Effects of the Isolated and Combined Ablation of Growth Hormone and IGF-1 Receptors in Somatostatin Neurons.Endocrinology · 2022Article
- Mice with gene alterations in the GH and IGF family.Pituitary · 2022Review
- Exercise in mice ameliorates high-fat diet-induced nonalcoholic fatty liver disease by lowering HMGCS2.Aging · 2021Article
- GH directly inhibits steatosis and liver injury in a sex-dependent and IGF1-independent manner.The Journal of endocrinology · 2021Article
- Tyrosine Hydroxylase Neurons Regulate Growth Hormone Secretion via Short-Loop Negative Feedback.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Adult-Onset Hepatocyte GH Resistance Promotes NASH in Male Mice, Without Severe Systemic Metabolic Dysfunction.Endocrinology · 2018Article
- 40 YEARS of IGF1: Understanding the tissue-specific roles of IGF1/IGF1R in regulating metabolism using the Cre/loxP system.Journal of molecular endocrinology · 2018Review
- Obesity and metabolic dysfunction severely influence prostate cell function: role of insulin and IGF1.Journal of cellular and molecular medicine · 2017Article
- Hypothalamic growth hormone receptor (GHR) controls hepatic glucose production in nutrient-sensing leptin receptor (LepRb) expressing neurons.Molecular metabolism · 2017Article
- Obesity- and gender-dependent role of endogenous somatostatin and cortistatin in the regulation of endocrine and metabolic homeostasis in mice.Scientific reports · 2016Article
- Altered somatotroph feedback regulation improves metabolic efficiency and limits adipose deposition in male mice.Metabolism: clinical and experimental · 2016Article
- In1-ghrelin splicing variant is overexpressed in pituitary adenomas and increases their aggressive features.Scientific reports · 2015Article
- Differential impact of selective GH deficiency and endogenous GH excess on insulin-mediated actions in muscle and liver of male mice.American journal of physiology. Endocrinology and metabolism · 2014Article
- Elevated GH/IGF-I promotes mammary tumors in high-fat, but not low-fat, fed mice.Carcinogenesis · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 3 countries.
Funding
Abstract
A unique mouse model was developed with elevated endogenous GH (2- to 3-fold) and IGF-I (1.2- to 1.4-fold), due to somatotrope-specific Cre-mediated inactivation of IGF-I receptor (IgfIr) and insulin receptor (Insr) genes (IgfIr,Insr(rGHpCre), referred to as HiGH mice). We demonstrate that the metabolic phenotype of HiGH mice is diet dependent and differs from that observed in other mouse models of GH excess due to ectopic heterologous transgene expression or pituitary tumor formation. Elevated endogenous GH promotes lean mass and whole-body lipid oxidation but has minimal effects on adiposity, even in response to diet-induced obesity. When caloric intake is moderated, elevated GH improves glucose clearance, despite low/normal insulin sensitivity, which may be explained in part by enhanced IGF-I and insulin output. However, when caloric intake is in excess, elevated GH promotes hepatic lipid accumulation, insulin resistance, hyperglycemia, and ketosis. The HiGH mouse model represents a useful tool to study the role endogenous circulating GH levels play in regulating health and disease.
Indexed as
Identifiers
What OpenQuestion holds
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.