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Context: Non-alcoholic fatty liver disease (NAFLD) is a leading causes of liver-related morbidity and mortality. While data on acromegaly, a state of chronic growth hormone (GH)/insulin-like growth factor I (IGF-I) excess, suggest an inverse relationship with intrahepatic lipid (IHL) content, less is known about the impact of the GH/IGF-I axis on IHL, lipid composition, and phosphor metabolites in individuals without disorders of GH secretion.
Objective: The aim was to investigate the relation between activity of the GH/IGF-I axis and IHL content and phosphor metabolism.
Methods: We performed a cross-sectional study in 59 otherwise metabolically healthy individuals (30 females), of which 16 met the criteria of NAFLD with IHL of ≥5.6%. The GH/IGF-I axis was evaluated in a fasting state and during an oral glucose tolerance test (OGTT). Insulin sensitivity was estimated by validated indices. IHL, lipid composition (unsaturation index), and phosphate metabolites were analyzed by using 1H/31P magnetic resonance spectroscopy.
Results: In the overall cohort (40.6 ± 15 years; body mass index: 24.5 ± 3 kg/m2; IGF-I: 68.0 ± 17% upper limit of normal), fasting GH (R = -0.31; P = .02), GH during oral glucose tolerance test (R = -0.51; P < .01), and IGF-I (R = -0.28; P = .03) inversely correlated with IHL. GH levels during OGTT were significantly lower in NAFLD than in controls (47.7 [22; 143] ng/mL/min vs 16.8 [7; 32] ng/mL/min; P = .003). GH/IGF-I axis activity correlated with lipid composition and with phosphor metabolites. In multiple regression analysis, the GH/IGF-I axis activity was a strong predictor for IHL and lipid composition independent from insulin sensitivity.
Conclusion: GH/IGF-I axis activity impacts hepatic lipid and phosphate metabolism in individuals without disorders in GH secretion. Lower GH axis activity is associated with higher IHL and an unfavorable lipid composition, probably mediated by changes in hepatic energy metabolism.
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http://dx.doi.org/10.1210/clinem/dgad206 | DOI Listing |
Endocr Pract
September 2025
Departments of Neuroendocrinology and Neurology, Barrow Pituitary Center, Barrow Neurological Institute, University of Arizona College of Medicine and Creighton University School of Medicine, Phoenix, Arizona. Electronic address:
Objective: Growth hormone (GH) is essential for growth and bone metabolism. This article reviews preclinical data that has shaped our understanding of the mechanisms underpinning the effects of GH on bone beyond the downstream activation of insulin-like growth factor-I (IGF-I) generation and summarizes the clinical data of GH deficiency (GHD) and acromegaly on bone health parameters and fracture risk.
Methods: A literature search was conducted on PubMed using the following key words: GH, IGF-I, bone, GHD, and acromegaly.
Mol Biol Rep
February 2025
Department of Cell and Molecular Biology and Microbiology, Faculty of Biological Science and Technology, University of Isfahan, Isfahan, Iran.
Growth hormone (GH) is a key polypeptide hormone secreted by somatotroph cells in the anterior pituitary gland, essential for postnatal growth, metabolism, and systemic homeostasis. Its secretion is regulated by hypothalamic neuropeptides, including GH-releasing hormone and somatostatin. GH exerts effects through direct interaction with the growth hormone receptor and indirect pathways mediated by the GH-IGF-I axis.
View Article and Find Full Text PDFRev Endocr Metab Disord
June 2025
Interdisciplinary Stem Cell Institute, University of Miami Miller School of Medicine, Biomedical Research Building, 1501 N.W. 10th Avenue, Room 908, Miami, FL, 33136, USA.
Growth hormone (GH)-releasing hormone (GHRH), a hypothalamic peptide initially characterized for its role in GH regulation, has gained increasing attention due to its GH-independent action on peripheral physiology, including that of the cardiovascular system. While its effects on the peripheral vasculature are still under investigation, GHRH and synthetic agonists have exhibited remarkable receptor-mediated cardioprotective properties in preclinical models. GHRH and its analogs enhance myocardial function by improving contractility, reducing oxidative stress, inflammation, and offsetting pathological remodeling.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
January 2025
Department and Clinic of Endocrinology, Diabetes and Isotope Therapy, Wroclaw Medical University, Wrocław, Poland.
Front Endocrinol (Lausanne)
December 2024
Department of Endocrinology, Odense University Hospital, Odense, Denmark.
Growth hormone (GH) is the key regulator of insulin-like growth factor I (IGF-I) generation in healthy states. However, portal insulin delivery is also an essential co-player in the regulation of the GH/IGF-I axis by affecting and regulating hepatic GH receptor synthesis, and subsequently altering hepatic GH sensitivity and IGF-I generation. Disease states of GH excess (e.
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