Is Type 2 Diabetes a Glycogen Storage Disease of Pancreatic β Cells?

被引：70

作者：

Ashcroft, Frances M. ^{[1
,2
]}

Rohm, Maria ^{[1
,2
]}

Clark, Anne ^{[3
]}

Brereton, Melissa F. ^{[1
,2
]}

机构：

[1] Univ Oxford, Dept Physiol Anat & Genet, Parks Rd, Oxford OX1 3PT, England

[2] Univ Oxford, OXION, Parks Rd, Oxford OX1 3PT, England

[3] Univ Oxford, Oxford Ctr Diabet Endocrinol & Metab, Churchill Hosp, Oxford OX3 7LJ, England

来源：

CELL METABOLISM | 2017年 / 26卷 / 01期

基金：

欧洲研究理事会; 英国惠康基金;

关键词：

INSULIN-RELEASE; GLUCOSE; METABOLISM; ACCUMULATION; ISLETS; GENE; AUTOPHAGY; SYNTHASE; PHOSPHORYLASE; EXPRESSION;

D O I：

10.1016/j.cmet.2017.05.014

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Elevated plasma glucose leads to pancreatic beta cell dysfunction and death in type 2 diabetes. Glycogen accumulation, due to impaired metabolism, contributes to this "glucotoxicity" via dysregulated biochemical pathways promoting b cell dysfunction. Here, we review emerging data, and re-examine published findings, on the role of glycogen in b cells in normoglycemia and in diabetes.

引用

页码：17 / 23

页数：7

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