Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2026) 117 P217 | DOI: 10.1530/endoabs.117.P217

SFEBES2026 Poster Presentations Reproductive Endocrinology (14 abstracts)

A successful case of obesity pharmacotherapy reversing male infertility recovery

Masato Ahsan 1,2 , Amy Morrison 1,2 , Shailesh Gohil 1,2 , Miles Levy 1,2 & Narendra L Reddy 1,2


1The University Hospitals of Leicester, Leicester, United Kingdom; 2University of Leicester, Leicester, United Kingdom


Introduction: Obesity-related functional hypogonadotropic hypogonadism is increasingly recognized as a significant contributor to male subfertility, manifesting impairment in semen parameters and hormonal disruptions. Treatment options remain limited, underscoring an unmet clinical need. We present a case demonstrating significant fertility improvement with targeted obesity pharmacotherapy.

Case: A 42-year-old man presented with a 3-year history of infertility, obesity (BMI 40.6; 123 kg), T2DM, and erectile dysfunction (ED). Evaluation showed hypogonadotropic hypogonadism (FSH 6.9, LH 4.9 IU/l), low testosterone (3.2), low SHBG (19), and normal remaining pituitary function. Semen analysis confirmed azoospermia. He lost 6.3 kg on Semaglutide (Ozempic) over 3 months and further 10 kg on Tirzepatide (Mounjaro), reducing BMI from 40.6 to 32.1 in 8 months. ED symptoms and semen parameters improved. His partner achieved natural conception 8 months after obesity pharmacotherapy, resulting in a healthy baby girl.

Table 1. Comparison of clinical characteristics of AI and non-AI group
ParameterBaselinePost-weight lossNormal range
BMI40.632.118.5-24.9 kg/m2
Testosterone3.27.411.5-54.5 nmol/l
LH4.921.5-9.3 iu/l
FSH6.94.91.4-18.1 iu/l
SHBG192211.5-54.5 nmol/l
Inhibin B111.525-325 pg/ml
Semen analysis
pH88.17.2-8.0
Volume1.55.31.4 ml
Concentration03116million/ml
Morphology02%4%
Motility039%> 30%
Total sperm number0164.3> 40million

Discussion: Reduced fat mass lowers aromatase activity, decreasing androgen-to-oestrogen peripheral conversion and improving the testosterone–oestrogen ratio essential for spermatogenesis. Direct stimulation of testicular receptors by GIP and GLP-1 enhances Leydig cell function, promoting testosterone synthesis and spermatogenesis. We are currently recruiting for a male fertility sub-study investigating the impact of Tirzepatide-induced weight loss on male reproductive health.

Learning points: 1. Fat mass reduction & potential direct stimulation of GLP1 & GIP receptors can improve male fertility outcomes in obesity induced hypogonadism. 2. GLP-1 or dual GLP-1/GIP agonists may offer therapeutic option for male infertility.

Volume 117

Society for Endocrinology BES 2026

Harrogate, United Kingdom
02 Mar 2026 - 04 Mar 2026

Society for Endocrinology 

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