Hormonal
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.
If you are on long-term steroid medication or have high chronic cortisol levels, do not expect fat loss from stress-induced lipolysis. Instead, focus on managing insulin levels and caloric intake, as the hormonal environment promotes fat storage in the abdomen and liver through increased synthesis and cell differentiation, not just calorie burning.
it appears to be a paradox that the acute lipolytic effect of glucocorticoids is not manifest in long-term weight loss in humans... there is marked redistribution of body fat, with accumulation in the depots in the abdomen... Glucocorticoids increase rates of hepatic DNL contributing to VLDL... Glucocorticoids promote the differentiation of pre-adipocytes into mature adipocytes
Why this rating
Based on a comprehensive review of in vivo human studies, in vitro data, and clinical observations of 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
More from this paper
- Glucocorticoids promote hepatic de novo lipogenesis (DNL) and VLDL secretion, contributing to hepatic steatosis and increased circulating triglycerides in metabolic syndrome.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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