Disentangling the impact of obesity on reproductive, metabolic and adipokine profiles in women with or without PCOS

Nyunt Sandhi W; Bijal Patel; Yeung Arthur C; Jovanna Tsoutsouki; Kanyada Koysombat; Megan Young; Agathoklis Efthymiadis; Patrick McGown; Aaran Patel; Aureliane Pierret; Elizabeth Daniels; Maria Phylactou; Mills Edouard G; Comninos Alexander N; Ali Abbara; Dhillo Waljit S

doi:10.1530/endoabs.117.OP7.4

OP7.4

Prev Next

Section Contents Cite

Endocrine Abstracts (2026) 117 OP7.4 | DOI: 10.1530/endoabs.117.OP7.4

SFEBES2026 Oral Poster Presentations Reproductive Endocrinology (4 abstracts)

Disentangling the impact of obesity on reproductive, metabolic and adipokine profiles in women with or without PCOS

Sandhi W Nyunt ^1,2 , Bijal Patel ^1,2 , Arthur C Yeung ^1,2 , Jovanna Tsoutsouki ^1,2 , Kanyada Koysombat ^1,2 , Megan Young ^2,1 , Agathoklis Efthymiadis ^1,2 , Patrick McGown ^1,2 , Aaran Patel ^1,2 , Aureliane Pierret ^1,2 , Elizabeth Daniels ^1,2 , Maria Phylactou ^1,2 , Edouard G Mills ^1,2 , Alexander N Comninos ^1,2 , Ali Abbara ^1,2 & Waljit S Dhillo ^1,2

Author affiliations

¹Imperial College London, London, United Kingdom; ²Imperial College Healthcare NHS trust, London, United Kingdom

Background: Obesity and polycystic ovary syndrome (PCOS) frequently co-exist, however whilst PCOS is associated with increased hypothalamic GnRH neuronal pulsatility, animal models suggest that obesity is associated with reduced hypothalamic function. Dissecting the impact of obesity on reproductive, metabolic and adipokine pathways is essential to understand reproductive dysfunction in women.

Methods: We investigated reproductive, metabolic and adipokine profiles in 131 women. Overall, 25 of 76 women with PCOS had obesity, and 9 of 55 healthy eugonadal women with regular menstrual cycles had obesity. Follicular-phase bloods were analysed for reproductive hormones (LH, FSH, oestradiol, AMH, SHBG, total and free testosterone), metabolic markers (insulin, HOMA-IR, HbA1c, lipids) and adipokines (leptin, adiponectin, ghrelin). Group differences were assessed using Mann–Whitney U tests. Regression analyses (adjusted for age and ethnicity) evaluated associations between BMI and hormonal or metabolic outcomes.

Results: Adjusted models in women with PCOS revealed that BMI was inversely associated with LH (P = 0.03, R²=0.16), SHBG (P < 0.0001, R²= 0.38) and AMH (P = 0.04, R²=0.13), but positively associated with free testosterone (P < 0.0001, R²=0.34), fasting insulin (P = 0.0002, R²=0.35), HOMA-IR (P = 0.0012, R²=0.23) and lipids (P = 0.0001, R²=0.24). Leptin showed the strongest association with BMI (P < 0.0001, R²=0.82 in PCOS vs R²=0.48 in controls) while adiponectin and ghrelin declined with increasing BMI (both P = 0.001).

Conclusion: Obesity has a negative impact on reproductive hormone secretion including LH consistent with a mechanistic role in obesity-related hypogonadism. Reasons for the reduction in LH with obesity are multifactorial but include leptin resistance leading to decreased hypothalamic function and increased LH clearance. Increased GnRH neuronal activity in women with PCOS was most pronounced in those without obesity. These data support the independent impact of obesity on reproductive dysfunction in women with obesity that is distinct from PCOS.