Immune regulators of inflammation in obesity-associated type 2 diabetes and coronary artery disease.

OBJECTIVE

To summarize current work identifying inflammatory components that underlie associations between obesity-associated type 2 diabetes and coronary artery disease.

RESULTS

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.

CONCLUSIONS

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.