Research

Hormonal

Chronic testosterone treatment induces selective insulin resistance in subcutaneous adipocytes of women by impairing the phosphorylation of protein kinase C-zeta (PKCz) downstream of PI3-kinase, without affecting upstream IRS-1 or mitogenic signaling pathways.

For women with high androgen levels (such as in PCOS), excess testosterone can directly interfere with how fat cells respond to insulin. This happens not by blocking the main insulin signal, but by disrupting a specific downstream step (PKCz) required for glucose uptake. This suggests that managing androgen levels may be crucial for improving insulin sensitivity in these individuals.

GoodSupportsHIGH confidence
We conclude that (1) T, or an androgenic metabolite of T, induces insulin resistance in adipocytes of women, selective for metabolic signaling pathways; (2) this defect is via AR; and (3) the defect in signaling is independent of phosphatidyl-inositol 3-kinase activation and involves impaired phosphorylation of PKCz.
A. Corbould · Journal of Endocrinology · 2007

Why this rating

In vitro study using human cells; strong mechanistic evidence but lacks in vivo clinical trial confirmation of the specific pathway in humans.

Source

Chronic testosterone treatment induces selective insulin resistance in subcutaneous adipocytes of women

A. Corbould · Journal of Endocrinology · 2007

DOI 10.1677/joe.1.07070

mechanism_only · n=7Cited 183×
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DOI resolved against Crossref · corpus check 2026-06-10

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