Cardiometabolic Markers in Algerian Obese Subjects with and Without Type 2 Diabetes: Adipocytokine Imbalance as a Risk Factor

Abstract

Background/Objectives: An increase in body fat is linked to abnormalities in energy metabolism. We aimed at determining cardiometabolic risk in Algerian participants with obesity alone and with or without type 2 diabetes. The study measured the concentrations of circulating adipocytokines (leptin, adiponectin, resistin), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) to identify and examine how imbalances in adipocytokines may affect the parameters of cardiometabolic health. Methods: Algerian participants (n = 300) were recruited and divided into three groups: control, obese, and type 2 diabetics (with two sub-groups: with and without obesity). Insulin resistance was evaluated using HOMA-IR, while ELISA was used to measure adipocytokines. Atherogenic index in plasma (AIP), adiponectin-leptin ratio (ALR), and visceral adiposity index (VAI) were also assessed. One-way ANOVA was used to compare obesity and diabetes groups to the control one (p < 0.05). Logistic regression analysis was conducted to strengthen the robustness of statistical correlations. Results: Participants with reduced adiponectin-leptin ratio (ALR) and elevated levels of resistin, TNF-α, and IL-6 are found to be at higher risk of cardiovascular diseases. An imbalance in adipocytokine levels is caused by a decrease in adiponectin concentrations, and an increase in pro-inflammatory adipocytokines that maintain and exacerbate energy imbalance and induces hyperinsulinemia, exposing individuals to a high risk of cardiovascular diseases. Conclusions: Given that ALR is a functional biomarker of inflammation, insulin resistance, and adipose tissue dysfunction, targeting ALR could potentially be a therapeutic approach to coping with obesity-related cardiometabolic risks. Mediterranean diet, weight loss, and increased physical activity can be key components to promote healthy adipose tissue through the increase in ALR.