jdm

Journal of Diabetes & Metabolism

ISSN - 2155-6156

Abstract

Autophagic Dysfunction in Type 2 Diabetes Mellitus: Pathophysiology and Therapeutic Implications

Md. Tanjir Islam, Md. Sahab Uddin, Kamrun Nahar Lucky, Md. Manjurul Islam, Sheik Md. Saiful Islam, Md. Tanvir Kabir, Md. Farhad Hossain, Abdullah Al Mamun and Md. Shah Amran

Autophagy is an intracellular catabolic system by which cells degrade and recycle cytoplasmic constituents such as organelles and proteins through the lysosome-dependent path. Belgian biochemist, Christian de Duve coined the name "autophagy" in 1963. The identification of autophagy-related genes and finally discoveries of mechanisms for autophagy led to the award of the 2016 Nobel Prize in Medicine or Physiology to Japanese cell biologist, Yoshinori Ohsumi specializing in autophagy. Autophagy shows a crucial role in removing aggregated proteins and damaged organelles in order to conserve intracellular homeostasis. In order to control cellular homeostasis and disease states autophagy illustrates a vital role. For insulin resistant patients, insulin secretion and the mass of pancreatic β-cells is increased on account of alterations in the expression and activities of numerous proteins in β-cells. Simultaneously, autophagic activity seems to also be upgraded to adjust to the dynamic changes taking place in β-cells. Actually, faulty autophagy in β-cells recaps a number of features that are perceived in pancreatic islets in the course of the formation of type 2 diabetes mellitus (T2DM). In contrast, the dyregulation of autophagic function is also appears to happen in the β-cells of T2DM patients. Furthermore, autophagy deficiency is linked with the diabetes-related organ dysfunction. Therefore the intention of this study was to provide the impacts of autophagy based on current researches in the development of T2DM and to explore new therapeutic strategies for stopping T2DM pathogenesis.

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