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- W788176574 abstract "Glucose triggers insulin secretion trough a pathway that involves the cytoskeleton of the pancreas beta cell. Transient F-actin reorganization allows the insulin granules access to the plasma membrane for subsequent docking, fusion (mediated by SNARE complex) and insulin release. Small Rab-, Rasand Rho-family GTPases are involved in insulin secretion. Physiologically, a balance is maintained between the load of insulin translation into the endoplasmic reticulum (ER) and the folding capacity of the ER. An increased demand for insulin negatively affects the homeostasis of β cells and leads to ER stress. The PERK (protein kinase RNA-like endoplasmic reticulum kinase) pathway keeps the capacity of the pancreas beta cell to respond adequately to the ER stress. Chronically elevated glucose creates a huge stress on the β-cell which cannot be relieved and this lead to dysfunction. The best example is insulin resistance which leads to type 2 diabetes mellitus development. Fasting intact proinsulin and the ratio proinsulin/C peptide are biomarkers for β-cell dysfunction, insulin resistance and cardiovascular risk in type2 diabetes mellitus patients. Understanding better their significance is important for diabetes mellitus management and for finding new therapies aiming at preventing diabetes." @default.
- W788176574 created "2016-06-24" @default.
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- W788176574 date "2012-01-01" @default.
- W788176574 modified "2023-09-23" @default.
- W788176574 title "Physiological and dysfunctional secretion of insulin." @default.
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