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Type II diabetes is a heterogeneous syndrome results from the progressive defects of impairment of ß- cell insulin secretion and insulin resistant of the target tissues. It also increases due to the rising rate of obesity which involves the deficiency of insulin to compensate for insulin resistance by increasing insulin secretion . However it is increasingly clear that reductions in insulin sensitivity and ß- cell functions leads to the rise of type II diabetes . The normal pancreatic ß- cells displaying the remarkable response to nutrients and obesity – associated insulin resistance by the hyper secretion of insulin to maintain fuel homeostasis. But the cellular resistance unable to sustain the ß– cells compensatory response in type II diabetes . Although the cause of the metabolic deterioration is unknown, but several hypothesis have been proposed including mitochondrial dysfunction, oxidative stress, ER stress, and gluco-lipotoxicity [4, 5]. Recent studies with intensive investigations suggesting that elevated glucose along with circulating free fatty acids distributed especially from the intra abdominal fat are the major culprits of insulin resistance and beta cell dysfunction [6, 7]. But the underlying molecular and cellular mechanisms of gluco-lipotoxicity contribute to ß- cell dysfunction and loss in type II diabetes remains debated. A recent observation from experimental, clinical and genetic evidence suggests endoplasmic reticulum was responsible for molecular mechanism of gluco-lipotoxicity which may contribute to ß - cell dysfunction in type II diabetes [8, 9]. In this review, we discussed about the involvement of ER in gluco-lipotoxicity induced ß- cell dysfunction along with the brief involvement of mitochondria.
ER stress response
Adaptation to metabolic changes requires the high regulation and co-ordination of many homeostatic systems, since the quality and quantity of available nutrients does not temporally match their needs. Pancreatic ß - cells displaying remarkable response to nutrients by the balance between the anabolic hormone insulin and the catabolic hormone glucagon in order to maintain fuel homeostasis. For an appropriate response, the cells require the development of suitable sensors and signaling molecules, which integrates all these signals into an appropriate insulin secretory rate in order to maintain homeostasis.
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which translocates into the nucleus to induce ER stress response genes such as Bip . Inositol-requiring enzyme 1 is a type 1 transmembrane protein with endoribonuclease activity. Activated IRE1 catalyzes the splicing of X-box-binding protein 1 mRNA leads to translation of the active transcription factor XBP1 that induces the expression of genes required for protein folding, ER to Golgi transport and ERAD , Figure I.