The global increase in obesity-induced type 2 diabetes (T2DM) represents a burden for healthcare systems worldwide. Of particular concern is the increased morbidity associated with T2DM, in particular cardiovascular disease (CVD), leading to premature death. Obesity initially leads to the development of insulin resistance in adipose and other tissues. Insulin resistance is initially compensated by increased insulin secretion but ultimately insufficient insulin is produced and this leads to the development of T2DM. Understanding the causal mechanisms underpinning the development of obesity-induced insulin resistance may be beneficial in improving quality of life and life expectancy, with the potential for a major global impact on healthcare systems. There is abundant evidence from animal, human studies and in vitro studies to support functional roles for a number of inflammatory factors in obesity-induced insulin resistance. In this review we provide an overview of the evidence supporting a fundamental role for the fluid phase (in particular the complement system) and the cellular components of the innate immune system in the pathogenesis of obesity-induced insulin resistance and ultimately development of T2DM.
Keywords: Inflammation; Insulin resistance; Obesity; Type 2 diabetes.
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