Purpose of review: To summarize current work identifying inflammatory components that underlie associations between obesity-associated type 2 diabetes and coronary artery disease.
Recent findings: Recent studies implicate immune cells as drivers of pathogenic inflammation in human type 2 diabetes. Inflammatory lymphocytes characterize unhealthy adipose tissue, but regional adipose volume, primarily visceral and pericardial fat, also predict severity and risk for obesity-associated coronary artery disease. Having a greater understanding of shared characteristics between inflammatory cells from different adipose tissue depots and a more accessible tissue, such as blood, will facilitate progress toward clinical translation of our appreciation of obesity as an inflammatory disease.
Summary: Obesity predisposes inflammation and metabolic dysfunction through multiple mechanisms, but these mechanisms remain understudied in humans. Studies of obese patients have identified disproportionate impacts of specific T cell subsets in metabolic diseases like type 2 diabetes. On the basis of demonstration that adipose tissue inflammation is depot-specific, analysis of adiposity by waist-to-hip ratio or MRI will increase interpretive value of lymphocyte-focused studies and aid clinicians in determining which obese individuals are at highest risk for coronary artery disease. New tools to combat obesity-associated coronary artery disease and other comorbidities will stem from identification of immune cell-mediated inflammatory networks that are amenable to pharmacological interventions.