Indan Journal of Medical Research Indan Journal of Medical Research Indan Journal of Medical Research
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Year : 2016  |  Volume : 144  |  Issue : 4  |  Page : 515-524

Apoptosis, autophagy & endoplasmic reticulum stress in diabetes mellitus

1 Department of Internal Medicine, Erzincan University, Erzincan, Turkey
2 Division of Nephrology, Kırsehir Training and Research Hospital, Kırsehir, Turkey
3 Department of Internal Medicine, Necmettin Erbakan University, Meram School of Medicine, Konya, Turkey
4 Department of Reanimation & Anesthesiology, Erzincan University, Erzincan, Turkey

Correspondence Address:
Kultigin Turkmen
Department of Internal Medicine, Division of Nephrology, Necmettin Erbakan University, Meram School of Medicine, 42090, Konya
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-5916.200887

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The prevalence of diabetes mellitus (DM) is increasing secondary to increased consumption of food and decreased physical activity worldwide. Hyperglycaemia, insulin resistance and hypertrophy of pancreatic beta cells occur in the early phase of diabetes. However, with the progression of diabetes, dysfunction and loss of beta cells occur in both types 1 and 2 DM. Programmed cell death also named apoptosis is found to be associated with diabetes, and apoptosis of beta cells might be the main mechanism of relative insulin deficiency in DM. Autophagic cell death and apoptosis are not entirely distinct programmed cell death mechanisms and share many of the regulator proteins. These processes can occur in both physiologic and pathologic conditions including DM. Besides these two important pathways, endoplasmic reticulum (ER) also acts as a cell sensor to monitor and maintain cellular homeostasis. ER stress has been found to be associated with autophagy and apoptosis. This review was aimed to describe the interactions between apoptosis, autophagy and ER stress pathways in DM.

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