Authors: Elena Vasquez, Tariq Al-Hassan, Mei-Ling Chen
Journal: Frontiers in Metabolic Medicine and Clinical Nutrition (FMMCN), ISSN 3087-4866
Citation: FMMCN 1(1), 2024-01-31.
Type: Original Research
Background: Obesity-related insulin resistance (IR) is a key precursor to type 2 diabetes and metabolic disease. While adipose tissue inflammation is a well-established contributor, the role of mitochondrial dysfunction within adipocytes remains incompletely understood. This study aimed to investigate whether adipose tissue mitochondrial dysfunction independently drives IR in obesity, beyond the effects of inflammation and lipid accumulation.Methods: We conducted a cross-sectional analysis of 120 adults with obesity (BMI ≥30 kg/m²) and 60 lean controls. Adipose tissue biopsies were obtained from subcutaneous and visceral depots. Mitochondrial function was assessed via respirometry and citrate synthase activity. Insulin sensitivity was measured by hyperinsulinemic-euglycemic clamp. Adipose tissue inflammation was quantified by macrophage infiltration (CD68+ cells) and cytokine levels. Statistical analyses included multivariate regression and mediation models.Results: Obese individuals exhibited significantly lower mitochondrial respiratory capacity (state 3 respiration: 45.2 ± 12.1 vs. 72.8 ± 15.4 pmol O₂/s/mg, pConclusions: Adipose tissue mitochondrial dysfunction is a significant and partially independent driver of insulin resistance in obesity. These findings suggest that targeting mitochondrial health may offer therapeutic potential for improving metabolic outcomes in obesity.
mitochondrial dysfunction, adipose tissue, insulin resistance, obesity, inflammation, metabolic health