Growth hormone/insulin-like growth factor I axis in health and disease states: an update on the role of intra-portal insulin.
Level 5 - mechanism / opinion, no new human data
Narrative review of physiological and clinical mechanisms without systematic review or new empirical human data.
PubMed 39665021 · doi:10.3389/fendo.2024.1456195
What was done
Narrative review summarizing current understanding of how intra-portal insulin delivery to the liver regulates hepatic growth hormone (GH) receptor synthesis, GH sensitivity, and insulin-like growth factor-binding protein 1 (IGFBP-1) secretion across physiological, pathological, and pharmacological states.
What was found
The abstract reports conceptual and mechanistic relationships without numerical data: - Primary GH disorders (e.g., acromegaly, congenital isolated GH deficiency) show concordant shifts in GH, IGF-I, and insulin levels. - Altered intra-portal insulin delivery causes secondary discordance between GH and IGF-I levels. Elevated intra-portal insulin (e.g., obesity, Cushing's syndrome, glucocorticoid or GLP-1 receptor agonist treatment) and reduced intra-portal insulin (e.g., malnutrition, anorexia nervosa, type 1 diabetes mellitus) alter hepatic GH sensitivity. - Intra-portal insulin modulates hepatic IGFBP-1 secretion, altering free IGF-I levels and pituitary GH negative feedback.
Why it matters
Recognizing the impact of portal insulin on hepatic GH sensitivity provides a physiological basis for interpreting discordant GH and IGF-I levels in metabolic and endocrine disorders.
Limits
As a narrative review, this paper presents no original data, quantitative estimates, or systematic search criteria in the abstract. Clinical outcomes and diagnostic accuracy metrics were not assessed.
Cited by
- supports Growth hormone acts as a signal telling the liver to produce IGF-1.