ArticleThe Journal of clinical investigation2011
Abrogation of growth hormone secretion rescues fatty liver in mice with hepatocyte-specific deletion of JAK2.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 84 papers.
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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
84 citing papers in PubMed, 138 citations in OpenAlex.
- Growth Hormone Administration Improves Nonalcoholic Fatty Liver Disease in Overweight/Obesity: A Randomized Trial.The Journal of clinical endocrinology and metabolism · 2023Trial
- Acromegaly and Metabolic Dysfunction-Associated Steatotic Liver Disease: Clinical and Therapeutic Implications.Current obesity reports · 2026Review
- STAT1/3/5 Functions Driving Lipid and Energy Metabolism in Cancer and Immunity.International journal of molecular sciences · 2026Review
- Adult Growth Hormone Deficiency and Metabolic Dysfunction-Associated Steatotic Liver Disease.Current obesity reports · 2026Review
- Deletion of hepatic growth hormone receptor contributes to the pathogenesis of lean MAFLD by elevating CD36.Life metabolism · 2026Article
- Depletion of IGFALS Serum Level up to 3 Months After Cardiac Surgery, with Exploration of Potential Relationships to Surrogates of Organ Failures and Clinical Outcomes.Current issues in molecular biology · 2025Article
- Growth Hormone Replacement in Craniopharyngioma: Analysis of the Hypopituitary Control and Complications Study (HypoCCS).Journal of the Endocrine Society · 2025Article
- Liver-specific actions of GH and IGF1 that protect against MASLD.Nature reviews. Endocrinology · 2025 · on this mapReview
- GHRH-stimulated pituitary small extracellular vesicles inhibit hepatocyte proliferation and IGF-1 expression by its cargo miR-375-3p.Journal of nanobiotechnology · 2024Article
- Endocrine and cellular physiology and pathology of the insulin-like growth factor acid-labile subunit.Nature reviews. Endocrinology · 2024Review
- Article
- Functional role of Ash2l in oxLDL induced endothelial dysfunction and atherosclerosis.Cellular and molecular life sciences : CMLS · 2024Article
- Proteomic and metabolomic analysis of GH deficiency-induced NAFLD in hypopituitarism: insights into oxidative stress.Frontiers in endocrinology · 2024Article
- Direct and systemic actions of growth hormone receptor (GHR)-signaling on hepatic glycolysis, de novo lipogenesis and insulin sensitivity, associated with steatosis.Metabolism: clinical and experimental · 2023Article
- Growth hormone and nonalcoholic fatty liver disease.Immunometabolism (Cobham, Surrey) · 2023 · on this mapReview
- Alcohol, White Adipose Tissue, and Brown Adipose Tissue: Mechanistic Links to Lipogenesis and Lipolysis.Nutrients · 2023Review
- Review
- Short-Term Growth Hormone Administration Mediates Hepatic Fatty Acid Uptake and De Novo Lipogenesis Gene Expression in Obese Rats.Biomedicines · 2023Article
- Chi-Circ_0006511 Positively Regulates the Differentiation of Goat Intramuscular Adipocytes via Novel-miR-87/CD36 Axis.International journal of molecular sciences · 2022Article
- Growth hormone deficiency and NAFLD: An overlooked and underrecognized link.Hepatology communications · 2022Review
24 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedDosage error in article text
Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
Non-alcoholic fatty liver disease is associated with multiple comorbid conditions, including diabetes, obesity, infection, and malnutrition. Mice with hepatocyte-specific disruption of growth hormone (GH) signaling develop fatty liver (FL), although the precise mechanism underlying this finding remains unknown. Because GH signals through JAK2, we developed mice bearing hepatocyte-specific deletion of JAK2 (referred to herein as JAK2L mice). These mice were lean, but displayed markedly elevated levels of GH, liver triglycerides (TGs), and plasma FFAs. Because GH is known to promote lipolysis, we crossed GH-deficient little mice to JAK2L mice, and this rescued the FL phenotype. Expression of the fatty acid transporter CD36 was dramatically increased in livers of JAK2L mice, as was expression of Pparg. Since GH signaling represses PPARγ expression and Cd36 is a known transcriptional target of PPARγ, we treated JAK2L mice with the PPARγ-specific antagonist GW9662. This resulted in reduced expression of liver Cd36 and decreased liver TG content. These results provide a mechanism for the FL observed in mice with liver-specific disruption in GH signaling and suggest that the development of FL depends on both GH-dependent increases in plasma FFA and increased hepatic uptake of FFA, likely mediated by increased expression of CD36.
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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.