# Measuring Adipocytokines in Young Patients With Type 2 Diabetes Presenting to a Tertiary Care Centre in Upper Assam, India

## TL;DR

This study found that young, lean individuals with type 2 diabetes in India show signs of inflammation rather than obesity-related insulin resistance, suggesting different causes for diabetes depending on body weight.

## Contribution

The study identifies distinct inflammatory and metabolic profiles in lean versus obese young T2DM patients in Northeast India.

## Key findings

- Lean diabetics had higher adiponectin but elevated CRP and IL-6, indicating inflammation rather than insulin resistance.
- Obese diabetics showed low adiponectin and high leptin, reflecting adiposity-linked metabolic stress.
- CRP was the most influential predictor of diabetes risk, with a modest overall predictive accuracy of 33.3%.

## Abstract

Background

Type 2 diabetes mellitus (T2DM) in lean and young adults is emerging as a distinct phenotype in South Asia, often dissociated from obesity-driven insulin resistance. This study evaluated adipocytokines (adiponectin and leptin) and inflammatory markers (C-reactive protein (CRP) and interleukin-6 (IL-6)) in young T2DM and non-diabetic individuals across body mass index (BMI) categories to elucidate underlying metabolic and inflammatory profiles.

Methods

A hospital-based case-control analysis was conducted among 176 individuals (age and sex matched, 83 diabetics, 93 non-diabetics) aged 18-45 years (105 females, 71 males), drawn from the PHENOEINDY-2 cohort at Assam Medical College and Hospital, Dibrugarh. Participants were stratified into four BMI groups: underweight (<18.5 kg/m²), normal (18.5-24.9 kg/m²), overweight (25.0-29.9 kg/m²), and obese (>30 kg/m²). Serum adiponectin, leptin, IL-6, and high-sensitivity CRP (hs-CRP) were measured using enzyme-linked immunosorbent assay (ELISA)-based assays. Statistical comparisons employed t-tests, ANOVA, and regression modeling, adjusting for age and socioeconomic factors.

Results

Among diabetics, mean adiponectin was highest in the underweight group (3.44 ± 2.56 µg/mL) and declined with increasing BMI, showing a significant negative correlation with BMI (r = -0.65, P = 0.079). Leptin demonstrated a strong positive correlation with BMI (r = 0.77, P = 0.024), increasing progressively from underweight (0.54 ± 0.66 ng/mL) to obese participants (0.80 ± 0.96 ng/mL). CRP levels were markedly elevated in underweight diabetics (8.15 ± 11.9 mg/L) versus non-diabetics (2.19 ± 1.75 mg/L, P = 0.075), suggesting low-grade inflammation even in non-obese individuals. A positive association between CRP and BMI (r = 0.67, P = 0.012) was observed overall. IL-6 levels peaked among normal-weight (102.36 ± 179.5 pg/mL) and overweight diabetics (118.72 ± 163.38 pg/mL), without significant correlation with BMI (r = -0.12, P = 0.777), indicating adiposity-independent inflammation. Logistic regression incorporating all biomarkers yielded a modest predictive accuracy of 33.3%, with CRP emerging as the most influential predictor of diabetes risk, followed by IL-6. Scatter plots confirmed negative trends for adiponectin and positive associations for leptin and CRP with BMI, while IL-6 remained BMI-independent.

Interpretation

Lean diabetics exhibited distinct biochemical features - higher adiponectin but elevated CRP and IL-6 - supporting inflammation and β-cell dysfunction as key drivers over insulin resistance. In contrast, obese diabetics demonstrated low adiponectin and high leptin, reflecting adiposity-linked metabolic stress. The elevated inflammatory markers among lean diabetics highlight non-adipose origins of inflammation, possibly from hepatic or immune pathways.

Conclusions

This study underscores heterogeneity in T2DM pathophysiology across BMI categories in Northeast India. Inflammation, rather than adiposity, may underlie dysglycemia among lean individuals, while adipokine imbalance predominates in obesity-associated diabetes. Integrating adiponectin, CRP, and IL-6 into risk assessment could refine screening for atypical or lean T2DM phenotypes. Future longitudinal and genetic studies are warranted to dissect the contribution of developmental and ethnic factors unique to this population.