Acromegaly and Metabolic Dysfunction-Associated Steatotic Liver Disease: Clinical and Therapeutic Implications

06/08/2026

AI Summary

Growth hormone can reduce hepatic steatosis, inflammation and fibrosis via hepatocyte and IGF-1 mediated stellate cell senescence, yet may increase hepatocellular carcinoma risk.
Acromegaly associates with low MASLD and VAT yet high insulin resistance, contradicting the usual positive correlation between insulin resistance and hepatic steatosis.
Treatment of acromegaly commonly increases hepatic steatosis and visceral fat despite lowering insulin resistance; long-term effects on hepatic inflammation and fibrosis remain unknown.

AI Summary

PURPOSE OF REVIEW: This narrative review aims to critically summarize available data on the association between adult acromegaly and metabolic dysfunction-associated steatotic liver disease (MASLD), with a particular focus on clinical associations and treatment implications.

From a clinical perspective, individuals with acromegaly have low rates of hepatic steatosis and visceral adipose tissue (VAT), but high insulin resistance (IR), which contradicts the generally observed positive association between IR and VAT or hepatic steatosis.

Acromegaly is associated with IR, type 2 diabetes mellitus, hypertension and cardiovascular disease; however, acromegaly is inversely associated with VAT and MASLD.

Basic summary

Curr Obes Rep. 2026 Aug 5;15(1):69. doi: 10.1007/s13679-026-00747-y.

ABSTRACT

RECENT FINDINGS: From a pathophysiological perspective, growth hormone (GH) may improve hepatic steatosis, inflammation, and fibrosis by acting directly on hepatocytes and indirectly (through insulin-like growth factor-1) on hepatic stellate cells, thereby inducing their senescence. Nonetheless, GH excess may also favor the development of hepatocellular carcinoma, possibly through mechanisms unrelated to hepatic fibrosis. From a clinical perspective, individuals with acromegaly have low rates of hepatic steatosis and visceral adipose tissue (VAT), but high insulin resistance (IR), which contradicts the generally observed positive association between IR and VAT or hepatic steatosis. By contrast, limited data do not support lower rates of hepatic fibrosis in acromegaly, possibly because GH excess is controlled after diagnosis. From a therapeutic perspective, published evidence, derived mainly from case series, suggests that surgical or pharmacological management of acromegaly increases hepatic steatosis and VAT, despite decreasing IR. However, the long-term effect of acromegaly control on hepatic inflammation and fibrosis remains largely unknown. Acromegaly is associated with IR, type 2 diabetes mellitus, hypertension and cardiovascular disease; however, acromegaly is inversely associated with VAT and MASLD. Further mechanistic and clinical studies are warranted to better elucidate the intriguing association between acromegaly and MASLD.

PMID:42554920 | DOI:10.1007/s13679-026-00747-y

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