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Adipose Tissue_Appetite_and Obesity

SAT-698 - Association of Sex Hormone Binding Globulin and Sex Hormones with Metabolic Dysfunction-Associated Steatotic Liver Disease and/or Non-Alcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis

Saturday, June 13, 2026
9:30 AM - 4:30 PM CT
Location: ENDOExpo; Poster Floor


Introduction:
Metabolic dysfunction-associated liver disease (MASLD) or non alcoholic liver disease (NAFLD) are among the leading causes of chronic liver disease worldwide. Sex hormone-binding globulin (SHBG) and endogenous sex hormones have been shown to play an important role in hepatic steatosis. We conducted a systematic review and meta-analysis to evaluate the association between these sex hormones, MASLD, and NAFLD.

Methods:
A comprehensive systematic literature search was conducted on PubMed, Cochrane CENTRAL, Embase, and Scopus from inception through September 2025. Studies showing an association between SHBG or endogenous sex hormones with either MASLD or NAFLD were included. Pooled odds ratios (OR) with 95% confidence intervals (CI) were calculated using a generalized linear model (GLM) on Rstudio (v4.1.1). Statistical significance was defined as a p-value < 0.05.

Results:
A total of 23 observational studies comprising 31,144 patients (18,685 in the MASLD/MASH group and 12,459 in the control group) were included in this meta-analysis. SHBG was significantly associated with reduced odds of MASLD/MASH (OR: 0.53; 95% CI: 0.36-0.79; p=0.0016) [Figure 1]. Among sex hormones, Estrogen demonstrated a modest but significant protective association (OR: 0.96; 95% CI: 0.93-1.00; P=0.0252) [Figure 2]. No significant associations were observed with testosterone (OR: 1.18; 95% CI: 0.85-1.62; p=0.3183), luteinizing hormone (OR: 1.09; 95% CI: 0.83-1.45; p=0.5351), or follicle-stimulating hormone (OR: 0.79; 95% CI: 0.46-1,38; p=0.4131).

Conclusion:
Our study suggests that SHBG and Estrogen are significantly associated with lower odds of MASLD/MASH, suggesting a potential protective endocrine mechanism. However, testosterone, follicle-stimulating hormone, and luteinizing hormone were not associated with disease risk. Further prospective studies and trials are required to elucidate causal pathways and clinical utility in risk stratification and to generate more robust evidence of the outcomes among patients with either MASLD or MASH.

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