
Role and mechanism of pancreatic β‐cell death in diabetes: The emerging role of autophagy
Author(s) -
Kim KyoungAh,
Lee MyungShik
Publication year - 2010
Publication title -
journal of diabetes investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.089
H-Index - 50
eISSN - 2040-1124
pISSN - 2040-1116
DOI - 10.1111/j.2040-1124.2010.00054.x
Subject(s) - autophagy , programmed cell death , medicine , diabetes mellitus , apoptosis , mechanism (biology) , type 2 diabetes , insulin resistance , pancreatic islets , type 1 diabetes , cell metabolism , cause of death , cell , bioinformatics , microbiology and biotechnology , islet , endocrinology , disease , biology , metabolism , biochemistry , philosophy , epistemology
Pancreatic β‐cell failure resulting from decreased β‐cell mass or dysfunction is the ultimate step towards most types of diabetes. Even if insulin resistance exists, diabetes does not develop unless pancreatic β‐cell function or its adaptation is compromised. Classically, two types of cell death (apoptosis and necrosis) have been studied in the diabetes field. Recently, a third type of cell death (autophagy, sometimes called type 2 programmed cell death in comparison with apoptosis, type 1 programmed cell death) and its pathophysiological role have been recognized and are being investigated. In the present review, we will discuss the role of various types of cell death in the development of type 1 and type 2 diabetes. Specifically, we will briefly cover recent progress regarding the role of autophagy in diabetes, which is becoming a hot topic in diabetes and metabolism. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2010.0054.x, 2010)