Adipose Tissue_Appetite_and Obesity

SUN-686 - Adipose-HPG Axis Coupling: Meta-Analysis of Obesity and Luteinizing Hormone Tone in 36,079 Individuals

Sunday, June 14, 2026

9:00 AM - 4:00 PM CT

Location: ENDOExpo; Poster Floor

Abstract Poster Presenter(s)

UC

Uliana Cheliadinova, MD

Instructor
ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI
New York, NY, United States

Co-Author(s)

DV

Darya Vasilyeva, MD

Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, NY, USA
NEW YORK, New York, United States
FK

Funda Korkmaz, MD

Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, NY, USA
New York, New York, United States
JR

Jensen Reckhow, MD (she/her/hers)

Reproductive Endocrinology and Infertility Fellow
Department of Obstetrics, Gynecology, and Reproductive Science, Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, NY, USA
New York, New York, United States
KI

Kseniia Ievleva, MD, PhD

Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, NY, USA
New York, New York, United States
OM

Ofer Moldavski, PhD

Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, NY, USA
New York, NY, New York, United States

Senior Author/Primary Investigator(s)

TY

Tony Yuen, PhD

Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, NY, USA
NEW YORK, New York, United States
MZ

Mone Zaidi, MD, PhD (he/him/his)

Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, NY, USA
New York, NY, New York, United States
DL

Daria Lizneva, MD, PhD

Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, NY, USA
NEW YORK, New York, United States

Co-Author(s)

AG

Anisa Gumerova, MD, PhD (she/her/hers)

Institute for Translational Medicine and Pharmacology, Icahn School of Medicine at Mount Sinai, New York, NY, USA
New York, NY, New York, United States

Disclosure(s):

Uliana Cheliadinova, MD: No financial relationships to disclose

Background: Obesity is increasingly recognized as a chronic metabolic–endocrine state that alters neuroendocrine axes. Gonadotropins integrate metabolic, hypothalamic, and steroidal signals, and accumulating evidence suggests bidirectional communication between the hypothalamic–pituitary–gonadal (HPG) axis and adipose tissue. Whether obesity and gonadotropin tone systematically reshape one another across sex and life stages remains unclear.

Objective: To synthesize human evidence on the association between obesity and basal or stimulated luteinizing hormone (LH) secretion and to examine context-specific modifiers including sex, menopausal status, adolescence, and reproductive comorbidity.

Methods: A PRISMA-2025–compliant systematic review and meta-analysis (PROSPERO CRD420250636001) was conducted using PubMed, Embase, and Cochrane Library through August 2025. Eligible studies compared obese vs non-obese groups and reported mean LH (primary outcome), LH/FSH ratio, or peak LH after GnRH stimulation (secondary outcomes). Standardized mean differences (Hedges’ g) and mean differences (MDs) were pooled using random-effects models. Prespecified stratifications examined sex, life stage (adolescents, reproductive-age, and menopausal), and PCOS/infertility. Risk of bias was assessed via structured 11-item tool; publication bias via Egger’s test.

Results: From 16,863 records, 217 studies (n=36,079; 366 comparisons) met eligibility. Obese women showed lower basal LH versus non-obese (SMD: −0.24 [95%CI: −0.32, −0.17]), consistent across adolescents, reproductive-age, and menopausal groups, with strongest suppression in menopause (SMD: −0.58 [−0.77, −0.38]; I²=0%). PCOS amplified suppression (SMD: −0.30 [−0.41, −0.19]). In men, overall effects were non-significant (SMD: −0.17 [−0.35, 0.01]), but obese men without reproductive comorbidities demonstrated LH suppression (SMD: −0.43 [−0.65, −0.21]), suggesting obesity’s metabolic effects on the HPG axis are present in both sexes. Peak LH post-GnRH was significantly lower in obese girls with precocious puberty (SMD: −0.26 [−0.38, −0.13]). LH/FSH ratio decreased in obese PCOS women (MD: −0.16 [−0.27, −0.06]) but not healthy women. Low-risk-of-bias analyses confirmed primary findings.

Conclusions: Obesity suppresses LH in women across life stages, with amplification in menopause and PCOS. Healthy men show comparable suppression, whereas compensatory mechanisms in infertile cohorts may obscure population effects. Critically, adipose tissue expresses functional LH receptors, suggesting gonadotropins may reciprocally influence adipose biology. Together, these findings bridge metabolic and reproductive endocrinology and highlight the HPG axis as a bidirectional integrator of metabolic state.

*Unless otherwise noted, all abstracts presented at ENDO must not be released to the press or the public until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.*