The epidemic of overweight and obesity is a major problem because of the plethora of health and economic issues that it induces. Key among these is the sharply increasing prevalence of type 2 diabetes (T2D) and cardiovascular disease. The development of T2D is characterised by two processes: 1) insulin resistance, resulting from impaired insulin signalling and leading to an increased demand for insulin, which must be met by increased insulin production by pancreatic beta-cells (compensatory beta-cell function); and 2) beta-cell dysfunction, with T2D developing when the amount of insulin that is produced is insufficient to meet the demand. Overweight and obesity, especially in case of abdominal fat accumulation, are associated with systemic low-grade inflammation. This low-grade inflammation is characterised by, among other things, higher levels of circulating proinflammatory cytokines and fatty acids. These can interfere with normal insulin function and thereby induce insulin resistance, and have also been implicated in beta-cell dysfunction. This review focuses on the known and emerging relations between inflammation and T2D. We first discuss current views on the effects of fat distribution on adipose tissue inflammation and adipose tissue dysfunction. Next we focus on the detrimental roles of proinflammatory cytokines and fatty acids on insulin signalling and beta-cell function. In the last part of this review we provide some insight into novel players in (the initiation of) inflammation in overweight and obesity, and their effects on T2D and vascular dysfunction.
|Journal||Netherlands Journal of Medicine|
|Publication status||Published - May 2013|
- insulin resistance
- beta-cell dysfunction
- vascular dysfunction
- innate and adaptive immunity