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A different facet of type 2 diabetes was recognized in the early 80s with the demonstration of the “state of coagulation activation” and “endothelial dysfunction / activation” in not only type 2 diabetes but also in obesity. The discovery of tumor necrosis factor (TNF) alpha and its physiological role including many aspects of coagulation activation and endothelial dysfunction was later found to have a correlation with adiposity and type 2 diabetes. Further knowledge in the metabolic function of TNF and concomitant discovery of elevated cytokines released from adipose tissue suggested the integral involvement of inflammation in the pathogenesis of type 2 diabetes and obesity. The increased influx of monocytes in adipose tissue, an inflammatory state, elevates TNF alpha secretion leading to the induction of insulin resistance through the release of free fatty acids from visceral adipose tissue; furthermore, TNF alpha directly causes insulin receptor signaling dysfunction by shifting the phosphorylation residues. The fundamental question of why excess adiposity stimulates inflammatory response, thereby insulin resistance, lingered for a decade. The demonstration of free fatty acids (lauric, palmitic and stearic acid) engaging Toll Like Receptor 4 to stimulate innate immunity has some similarity to bacterial lipopolysacharides; providing the link of visceral adiposity to inflammatory syndrome. This article provides a historical review of the progression of knowledge in unmasking the inflammatory aspect in diabetes and visceral obesity, which were diseases often associated with hyperglycemia. In fact, it is the inflammatory aspect of the disease that governs the basic pathophysiology with complex interplays at the cross road of inflammation and metabolism.

The Crossroad of Inflammation and Diabetes: Role of Toll-Like Receptor