ECEESPE2025 ePoster Presentations Reproductive and Developmental Endocrinology (128 abstracts)
Circulating adipokine concentrations aid in distinguishing functional hypothalamic amenorrhoea and polycystic ovary syndrome in women presenting with oligo/amenorrhoea
Kanyada Koysombat 1,2 , Bijal Patel 1,2 , Arthur Yeung 1 , Maria Phylactou 1,2 , Jovanna Tsoutsouki 1 , Megan Young 1 , Sandhi Nyunt 1,2 , Aaran Patel 1,2 , Aureliane Pierret 1,2 , Elisabeth Daniels 1,2 , Ambreen Qayum 1,2 , Yusra Omar 1,2 , Pei Eng 1,2 , Edouard G Mills 1,2 , Simon Hanassab 1,3 , Channa Jayasena 1,2 , Tricia Tan 1,2 , Sophie Clarke 4 , Alexander Comninos 1,2 , Ali Abbara 1,2 & Waljit Dhillo 1,2
1Imperial College London, Department of Metabolism, Digestion and Reproduction, London, United Kingdom; 2Imperial College Healthcare NHS Trust, Department of Endocrinology, London, United Kingdom; 3Imperial College London, Department of Computing, London, United Kingdom; 4University College Hospitals NHS Foundation Trust, London, United Kingdom
JOINT2211
Introduction: Adipokines, such as leptin and adiponectin, are secreted from adipose tissue and signal to the hypothalamus to indicate sufficient energy availability, which is requisite for reproductive health. Leptin is a permissive signal for hypothalamic GnRH function. Functional hypothalamic amenorrhoea (FHA) is caused by insufficient energy availability and is a low leptin state. Indeed, leptin administration restores pulsatile LH secretion in FHA. Conversely, adiponectin levels decrease with bodyweight, especially central obesity with associated insulin resistance. Polycystic ovary syndrome (PCOS) is strongly associated with insulin resistance and central adiposity. Herein, we directly compare circulating leptin and adiponectin concentrations in women presenting with oligo/amenorrhoea due to either FHA or PCOS.
Methods: Women aged 18-35yrs were classified as Healthy (n = 47), FHA (n = 44), or PCOS (n = 73; stratified by BMI as lean [BMI:<25kg/m2; n = 33], overweight [BMI:25-30kg/m2; n = 15] or obese [BMI:>30kg/m2; n = 25]). Serum adiponectin and leptin were measured by DELFIA assay. Insulin and glucose were collected following an 8-hour overnight fast. Reproductive hormones were collected during the follicular phase, or following a progesterone-induced bleed in PCOS. Groups were compared by Kruskal-Wallis and associations assessed by linear regression.
Results: Leptin was positively related to BMI in all groups, whereas adiponectin was negatively related to BMI only in Healthy and PCOS groups. Despite similar BMI (Healthy 21.2, FHA 20.4, Lean PCOS 21.1kg/m2), women with FHA had lower leptin and higher adiponectin levels. Median (IQR) leptin (ng/ml) was: Healthy 12.50 (5.80-18.25), FHA 5.20 (3.05-8.78), Lean PCOS 8.90 (6.40-17.10) (P <0.0001); and adiponectin (mg/ml) was: Healthy 9.90 (7.80-13.30), FHA 14.05 (10.98-17.10), Lean PCOS 9.20 (7.10-10.90) (P <0.0001). Women with FHA were more insulin sensitive than Healthy and Lean PCOS groups (HOMA-IR 0.63 vs 1.05 and 0.94 respectively, P = 0.002). Adiponectin was inversely associated with HOMA-IR in Healthy (r=-0.06; r2=0.25, P = 0.002) and PCOS (r=-0.14; r2=0.18, P = 0.0004), but this relationship was reversed in FHA (r=+0.04; r2=0.18, P = 0.013). Adiponectin was inversely associated with free androgen index (FAI) (r=-0.32; r2=0.11, P = 0.005), whereas leptin was positively associated with FAI (r=+0.06; r2=0.22, P <0.0001) in PCOS. Adiponectin was positively associated with LH in PCOS (r=+0.26; r2=0.14, P = 0.001), but not in FHA. Leptin was positively associated with LH (r=+0.09; r2=0.14, P = 0.014) and oestradiol in FHA (r=+1.27; r2=0.14, P = 0.012), but negatively associated with LH in PCOS (r=-0.03; r2=0.10, P = 0.007).
Conclusion: These data highlight the divergent interaction between adipokines and reproductive/metabolic markers in women with FHA and PCOS, providing novel insights into the value of adipokines in the assessment of women with oligo/amenorrhoea.
Volume 110
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