What are the effects of Growth Hormone (GH) on intermediary metabolism pathways?

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Last updated: May 23, 2025 • View editorial policy

From the Guidelines

Growth hormone has significant effects on intermediary metabolism pathways, primarily promoting anabolic processes while exerting anti-insulin or diabetogenic effects, as evidenced by its role in decreasing insulin sensitivity during puberty 1.

Effects on Carbohydrate Metabolism

  • Growth hormone decreases glucose uptake in peripheral tissues by reducing insulin sensitivity, as seen in hyperinsulinemic-euglycemic clamp studies demonstrating 30% lower insulin-mediated glucose disposal in adolescents compared to prepubertal children and young adults 1.
  • GH increases hepatic glucose production through glycogenolysis and gluconeogenesis, maintaining blood glucose levels during fasting.

Effects on Lipid Metabolism

  • Growth hormone enhances lipolysis in adipose tissue, increasing free fatty acid release and oxidation, which provides energy and spares glucose utilization.

Clinical Implications

  • The effects of growth hormone on intermediary metabolism pathways are crucial in understanding the development of type 2 diabetes in children and adolescents, particularly during puberty when insulin resistance is increased 1.
  • Close monitoring of glucose metabolism is advised when initiating GH therapy in patients with chronic kidney disease due to an increased risk of impaired glucose tolerance 2. ### Key Findings
  • Growth hormone secretion is most likely responsible for the insulin resistance during puberty, and both growth hormone secretion and insulin resistance decline with completion of puberty 1.
  • The adverse effect of obesity on glucose metabolism is evident early in childhood, with obese children being hyperinsulinemic and having 40% lower insulin-stimulated glucose metabolism compared to nonobese children 1.

From the Research

Effects of Growth Hormone on Intermediary Metabolism Pathways

  • Growth hormone (GH) has anabolic effects on glucose, lipid, and protein metabolism in human subjects 3
  • GH stimulates the release and oxidation of free fatty acids (FFA), leading to decreased glucose and protein oxidation and preservation of lean body mass (LBM) and glycogen stores 3
  • The most prominent metabolic effect of GH is a marked increase in lipolysis and FFA levels 3
  • GH has a counterregulatory effect on insulin, inducing insulin resistance via mechanisms involving increased FFA flux and uptake 3, 4
  • GH substitution in GH-deficient adults may worsen insulin resistance, but the GH-induced reduction in fat mass and increase in LBM may offset the insulin antagonistic actions of the hormone 5

Protein Metabolism

  • GH has modest effects on protein metabolism in the basal state, including increased protein synthesis and decreased breakdown at the whole body level and in muscle 3
  • During fasting and stress, the effects of GH on protein metabolism become more pronounced, with increased protein synthesis and decreased breakdown 3, 5
  • Lack of GH during fasting increases protein loss and urea production rates by approximately 50%, with a similar increase in muscle protein breakdown 3

Lipid Metabolism

  • GH mobilizes lipids by inhibiting lipoprotein lipase activity in adipose tissue and activating the hormone-sensitive lipase 5
  • Chronic stimulation of lipolysis by GH results in an increased flux of free fatty acids (FFAs) into systemic circulation, contributing to the development of insulin resistance 6
  • GH-induced lipolysis and impairment of insulin signaling are associated with deregulation of the FSP27-PPARγ axis, altering adipose tissue homeostasis and contributing to the development of insulin resistance and Type 2 diabetes 6

Clinical Implications

  • GH therapy requires close monitoring to prevent side effects like insulin resistance and metabolic complications 7, 4
  • The dose and timing of GH substitution should be tailored to minimize untoward effects, such as hypoglycaemia and hyperglycaemia 4

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.