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Cloettapreis_2014_Nr_42

19 Figure 1. Type 2 diabetes is caused by a continuous deterioration of the insulin-secretory capacity of pancreatic β-cells, which does not allow compensation for an increased peri- pheral insulin demand. In healthy individuals, insulin secretion by the pancreatic islet al- lows for normal glucose disposal in the insulin-sensitive tissues: fat, liver and adipose tissues (Upper panel). During prediabetes, genetic predisposition, overnutrition and phy- sical inactivity reduce the response to insulin-stimulated glucose uptake that is compen­ sated for by an increase in insulin production (Middle panel). In patients with type 2 dia- betes insulin secretion no longer compensates for the increased peripheral insulin demand (Lower panel). The progression from prediabetes to diabetes is largely dictated by changes in islet secretory capacity while insulin resistance remains relatively constant over time. (Reproduced from Donath MY: Nature reviews Drug discovery 2014, 13:465–76) ture IL-1β20, 21 (Figure 2). Increased insulin demand and production in- duces ER stress which also activates the inflammasome18 . Further­more,

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