MON-185 PCOS in Adolescent Girls versus Young Women: Similar Distribution of Body Fat, Different Severity of PCOS Phenotype

Abstract Disclosure: L. Ibanez: None. C. Garcia-Beltran: None. M. Andersen: None. F. Bas: None. J. Bassols: None. F. Darendeliler: None. F. Fanelli: None. E. Fröhlich-Reiterer: None. A. Gambineri: None. D. Glintborg: None. A. Lopez-Bermejo: None. S. Marin: None. B.M. Obermayer-Pietsch: None. R. Ødegård: None. P. Ravn: None. C. Salvador: None. E. Vanky: None. M. Yildiz: None. F.E. de Zegher: None. In essence, polycystic ovary syndrome (PCOS) is an endocrine-metabolic mode driven by ectopic fat [1]. It is unknown whether similar degrees of total, truncal, abdominal, visceral and hepatic adiposity associate to similar PCOS phenotypes in adolescent girls versus young women. The baseline data of an international PCOS intervention study [2] (www.spiomet4health.eu; Horizon 2020 grant 899671) offered an unanticipated opportunity to answer this question. Indeed, adolescent girls with PCOS (n=129; mean ± SD; 16 ± 2 yr) and young women with PCOS (n=183; 22 ± 1 yr) in this study happened to have similar measures of body adiposity: BMI 27 ± 5 vs 27 ± 5 kg/m2; total fat (by DXA) 29 ± 11 vs 28 ± 11 kg; truncal fat (by DXA) 14 ± 6 vs 13 ± 6 kg; non-truncal fat (by DXA) 15 ± 5 vs 15 ± 6 kg; abdominal thickness of subcutaneous fat (by MRI) 6 ± 2 vs 6 ± 2 cm; abdominal area of subcutaneous fat (by MRI) 218 ± 77 vs 219 ± 84 cm2; visceral fat (by MRI) 48 ± 29 vs 52 ± 34 cm2; and hepatic fat (by MRI-PDFF) 7 ± 5 vs 7 ± 2 %. However, the PCOS phenotype was more severe (all P<0.001) in adolescent girls than in young women: hirsutism score (modified Ferriman-Gallwey) 13 ± 6 vs 10 ± 6; SHBG 32 ± 18 vs 41 ± 20 nmol/L; free androgen index 6.8 ± 4.6 vs 4.9 ± 3.0; HOMA-IR 3.3 ± 3.2 vs 2.3 ± 2.5; mean serum insulin during oGTT 437 ± 456 vs 253 ± 218 pmol/L; HDL-cholesterol 1.3 ± 0.3 vs 1.6 ± 0.4 mmol/L. In conclusion, the baseline data of an intervention study disclosed unexpectedly that a similar fat distribution associates with a more severe PCOS phenotype in adolescent girls than in young women. A differential secretion of growth hormone may be among the mechanisms underpinning the difference in PCOS phenotype [3,4]. In order to reverse PCOS, measures to reduce adiposity and/or to redistribute fat may thus be even more relevant for adolescent girls than for young women. [1] Ibáñez L, de Zegher F. Adolescent PCOS: a postpubertal central obesity syndrome. Trends Mol Med. 2023; 29:354-363. [2] Garcia-Beltran C, et al. SPIOMET4HEALTH-efficacy, tolerability and safety of lifestyle intervention plus a fixed dose combination of spironolactone, pioglitazone and metformin (SPIOMET) for adolescent girls and young women with polycystic ovary syndrome: study protocol for a multicentre, randomised, double-blind, placebo-controlled, four-arm, parallel-group, phase II clinical trial. Trials. 2023; 24:589. [3] Morales AJ, et al. Insulin, somatotropic, and luteinizing hormone axes in lean and obese women with polycystic ovary syndrome: common and distinct features. J Clin Endocrinol Metab. 1996; 81:2854-64.[4] Ibáñez L, et al. Insulin sensitization early after menarche prevents progression from precocious pubarche to polycystic ovary syndrome. J Pediatr. 2004; 144:23-9. Presentation: Monday, July 14, 2025