Hormonal control of regional fat distribution.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic and in vitro literature without systematic search or new primary human trial data.
PubMed 9403318 · doi:10.1093/humrep/12.suppl_1.21
What was done
This narrative review summarizes in vitro cellular mechanisms and in vivo metabolic observations regarding the influence of cortisol, insulin, growth hormone, testosterone, and female sex steroids on lipoprotein lipase activity, lipolysis, and regional adipose tissue distribution.
What was found
The abstract reports no numerical data. Qualitatively, cortisol and insulin facilitate lipid accumulation by expressing lipoprotein lipase (LPL), whereas growth hormone (GH) and testosterone inhibit LPL and stimulate lipolysis. Cortisol and testosterone act via glucocorticoid and androgen receptors, with androgen receptor density reported to be higher in visceral than subcutaneous adipose tissue. Estrogens are reported to exert net metabolic effects similar to testosterone, though female sex steroids regulate adipose metabolism without direct specific cellular receptors.
Why it matters
It provides a mechanistic model linking specific endocrine profiles and depot-level receptor differences to clinical patterns of visceral versus subcutaneous body fat distribution.
Limits
The abstract provides no quantitative data, sample sizes, or effect estimates. Because this is an unsystematic narrative review, findings are subject to selection bias and rely heavily on in vitro mechanistic reasoning.
Cited by
- supports Elevated stress hormones mobilize glucose and lipids into the bloodstream which, if unused by tissues, deposit as ectopic visceral adipose tissue.