Abstract
Obesity is associated with tissue inflammation which is a crucial etiology of insulin resistance. This inflammation centers around circulating monocytes which form proinflammatory adipose tissue macrophages (ATM). Specific approaches targeting monocytes/ATM may improve insulin resistance without the adverse side effects of generalized immunosuppression. In this regard, a biomimetic membrane leukocyte processing device, called the selective cytopheretic device (SCD), was evaluated in an Ossabaw miniature swine model of insulin resistance with metabolic syndrome. Treatment with the SCD in this porcine model demonstrated a decline in circulating neutrophil activation parameters and monocyte counts. These changes were associated with improvements in insulin resistance as determined with intravenous glucose tolerance testing. These improvements were also reflected in lowering of homeostatic model assessment- (HOMA-) insulin resistant (IR) scores for up to 2 weeks after SCD therapy. These results allow for the planning of first-in-man studies in obese type 2 diabetic patients.
Highlights
Insulin resistance is the critical pathophysiological disorder in the vast majority of individuals with type 2 diabetes (T2D)
Obesity is associated with tissue inflammation which is recognized as a critical etiology of insulin resistance [1,2,3,4]
The results demonstrated, as measured with glucose tolerance testing (GTT), that, after selective cytopheretic device (SCD) Rx course, a dramatic improvement of insulin resistance in the animals was observed and persisted for at least 2 weeks, the longest time interval examined in this series of studies
Summary
Insulin resistance is the critical pathophysiological disorder in the vast majority of individuals with type 2 diabetes (T2D). Circulating white blood cell counts, including absolute neutrophil and monocyte counts, are elevated in diabetic patients compared to nondiabetics [5,6,7]. Do these cells of the innate immunologic system increase in absolute number, but they exist in a persistently activated state [8,9,10,11]. More specific approaches targeting monocyte/macrophage activity may be a novel intervention to diminish inflammation-induced insulin resistance without interfering with other immunologic activity, thereby avoiding adverse side effects
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