Protein Kinases Signaling in Pancreatic Beta-cells Death and Type 2 Diabetes.

Protein Kinases Signaling in Pancreatic Beta-cells Death and Type 2 Diabetes. Adv Exp Med Biol. 2021;1275:195-227 Authors: Engin AB, Engin A Abstract Type 2 diabetes (T2D) is a worldwide serious public health problem. Insulin resistance and β-cell failure are the two major components of T2D pathology. In addition to defective endoplasmic reticulum (ER) stress signaling due to glucolipotoxicity, β-cell dysfunction or β-cell death initiates the deleterious vicious cycle observed in T2D. Although the primary cause is still unknown, overnutrition that contributes to the induction of the state of low-grade inflammation, and the activation of various protein kinases-related metabolic pathways are main factors leading to T2D. In this chapter following subjects, which have critical checkpoints regarding β-cell fate and protein kinases pathways are discussed; hyperglycemia-induced β-cell failure, chronic accumulation of unfolded protein in β-cells, the effect of intracellular reactive oxygen species (ROS) signaling to insulin secretion, excessive saturated free fatty acid-induced β-cell apoptosis, mitophagy dysfunction, proinflammatory responses and insulin resistance, and the reprogramming of β-cell for differentiation or dedifferentiation in T2D. There is much debate about selecting proposed therapeutic strategies to maintain or enhance optimal β-cell viability for adequate insulin secretion in T2D. However, in order to achieve an ...
Source: Advances in Experimental Medicine and Biology - Category: Research Tags: Adv Exp Med Biol Source Type: research