Research
Hormonal
Glucocorticoids promote hepatic de novo lipogenesis (DNL) and VLDL secretion, contributing to hepatic steatosis and increased circulating triglycerides in metabolic syndrome.
Managing chronic steroid use or high cortisol is critical for liver health. Reducing glucocorticoid exposure can help lower liver fat production and improve lipid profiles, reducing the risk of fatty liver disease.
GoodSupportsHIGH confidence
Glucocorticoids increase rates of hepatic DNL contributing to VLDL, reducing the contribution from the stored cytosolic TAG pool, thereby potentially contributing to hepatic steatosis and to increased export of TAGs to adipose tissue depots
Why this rating
Supported by in vitro studies, tracer studies in humans, and observations in Cushing's syndrome.
Source
Glucocorticoids and fatty acid metabolism in humans: fuelling fat redistribution in the metabolic syndrome
David P. Macfarlane et al. · Journal of Endocrinology · 2008
DOI 10.1677/joe-08-0054
narrative_reviewCited 383×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Chronic glucocorticoid excess causes central fat redistribution and metabolic syndrome features despite acute lipolytic effects, primarily through increased de novo lipogenesis and adipocyte differentiation rather than sustained systemic lipolysis.Good
- Glucocorticoids promote adipocyte differentiation and increase adipocyte size, particularly in visceral and subcutaneous depots, contributing to fat redistribution in Cushing's syndrome.Good
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