Ovarian hyperandrogenism and its response to gonadotropin-re
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Insulin resistance (IR) is associated with polycystic ovaries and hyperandrogenism, but underpinning mechanisms are poorly understood, and therapeutic options limited.

This study aimed to characterize hyperandrogenemia and ovarian pathology in primary severe IR (SIR), using IR of defined molecular etiology to interrogate disease mechanism and to extend evaluation of gonadotropin-releasing hormone (GnRH) analogue therapy in SIR.

Female patients with SIR with documented serum total testosterone (TT) concentration were analyzed.

Results:
-- Among 185 patients with lipodystrophy, 65 with primary insulin signaling disorders, and 29 with idiopathic SIR, serum TT ranged from undetectable to 1562 ng/dL and free testosterone (FT) from undetectable to 18.0 ng/dL.

-- Higher TT but not FT in the insulin signaling subgroup was attributable to higher serum sex hormone binding globulin (SHBG) concentration.

-- Insulin correlated positively with SHBG in the insulin signaling subgroup, but negatively in lipodystrophy.

-- In 8/9 patients with available ovarian tissue, histology was consistent with polycystic ovary syndrome (PCOS).

-- In 6/6 patients treated with GnRH analogue therapy, gonadotropin suppression improved hyperandrogenic symptoms and reduced serum TT irrespective of SIR etiology.

Conclusively, SIR causes severe hyperandrogenemia and PCOS-like ovarian changes whether due to proximal insulin signaling or adipose development defects. A distinct relationship between IR and FT between the groups is mediated by SHBG. GnRH analogues are beneficial in a range of SIR subphenotypes.

Source: https://academic.oup.com/jcem/advance-article/doi/10.1210/clinem/dgab275/6253797?rss=1
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