Serum Leptin Levels and Obesity Severity: A Cross-Sectional Study Examining the Correlation with Anthropometric Indices, Metabolic Parameters, and Inflammatory Markers

Abstract

Background: Obesity is a global pandemic characterised by excessive adipose tissue accumulation and is strongly linked to cardiometabolic disease. Leptin, the primary adipokine secreted by white adipose tissue, serves as a central regulator of energy homeostasis; however, its precise quantitative relationship with graded obesity severity, sex-specific differences, and associated metabolic comorbidities remains incompletely characterised in South Asian populations. 

Aim: To evaluate the correlation between fasting serum leptin levels and obesity severity as defined by body mass index (BMI) category, and to identify independent clinical and biochemical predictors of serum leptin concentration in a hospital-based adult population. 

Methods: A cross-sectional, observational study was conducted among 240 adult participants (112 male, 128 female; age 18–65 years) attending the outpatient and metabolic clinic of a tertiary care hospital in Kolkata, India. Anthropometric measurements (BMI, waist circumference, waist-to-hip ratio) and fasting biochemical parameters including serum leptin (ELISA), fasting plasma glucose, lipid profile, high-sensitivity C-reactive protein (hs-CRP), and insulin were measured. Insulin resistance was estimated using HOMA-IR. Metabolic syndrome was defined per IDF 2009 criteria. Statistical analysis employed one-way ANOVA, Pearson and Spearman correlation analyses, and multiple linear regression with log-transformed leptin as the dependent variable.

Results: Mean serum leptin was significantly higher in females than males (34.0 ± 18.9 ng/mL vs. 14.3 ± 10.4 ng/mL; p < 0.001). A strong positive gradient in leptin levels was observed across BMI categories, ranging from 4.2 ± 1.4 ng/mL in underweight participants to 52.4 ± 14.8 ng/mL in Class III obesity (F = 148.3; p < 0.001). Pearson correlation confirmed a strong association between serum leptin and BMI (r = 0.81; p < 0.001), waist circumference (r = 0.76; p < 0.001), and HOMA-IR (r = 0.68; p < 0.001). On multiple regression, BMI (β = 0.048; p < 0.001), female sex (β = 0.384; p < 0.001), waist circumference (β = 0.011; p = 0.003), HOMA-IR (β = 0.072; p < 0.001), metabolic syndrome (β = 0.148; p = 0.006), and hs-CRP (β = 0.022; p = 0.041) emerged as significant  independent predictors (Adjusted R² = 0.697). 

Conclusion: Serum leptin levels rise progressively and significantly with increasing obesity severity, with pronounced sexual dimorphism. BMI, sex, central adiposity, and insulin resistance are the principal determinants of circulating leptin. These findings support the utility of serum leptin as a quantitative biomarker of obesity
burden and metabolic risk stratification.