Recent studies, including one from our own lab, report that different subpopulations of obese individuals display a variable inflammatory signature in their visceral adipose tissue that may contribute significantly to their risk for developing insulin resistance, type 2 diabetes, and other metabolic diseases. Understanding the molecular mechanisms and signaling pathways that lead to these differences in susceptibility to insulin resistance will equip us with important targets to help stem the tide of such debilitating diseases. Here we discuss an emerging theory that chronic, low-grade endotoxemia may represent a causal factor in obesity-related inflammatory states, and that diet-induced changes in the gut microbiome may be a key regulator of metabolic health. The implications to both disease prevention and to therapeutic intervention are also highlighted.
Keywords: endotoxemia; inflammation; insulin resistance; obesity; type 2 diabetes.