Diabetes Mellitus and the β Cell: The Last Ten Years

被引:722
作者
Ashcroft, Frances M. [1 ,2 ]
Rorsman, Patrik [2 ,3 ,4 ]
机构
[1] Univ Oxford, Henry Wellcome Ctr Gene Funct, Dept Physiol Anat & Genet, Oxford OX1 3PT, England
[2] Univ Oxford, OXION Ctr Ion Channel Studies, Oxford OX1 3PT, England
[3] Univ Oxford, Oxford Ctr Diabet Endocrinol & Metab, Oxford OX3 7LJ, England
[4] Churchill Hosp, Oxford NIHR Biomed Ctr, Oxford OX3 7LJ, England
基金
英国惠康基金;
关键词
K-ATP CHANNEL; GLUCAGON-LIKE PEPTIDE-1; GASTRIC BYPASS-SURGERY; SUBUNITS KIR6.2 KCNJ11; GLUCOSE-HOMEOSTASIS; INSULIN-SECRETION; ACTIVATING MUTATIONS; BARIATRIC SURGERY; PANCREATIC-ISLETS; CA2+ CHANNELS;
D O I
10.1016/j.cell.2012.02.010
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Diabetes is a major global problem. During the past decade, the genetic basis of various monogenic forms of the disease, and their underlying molecular mechanisms, have been elucidated. Many genes that increase type 2 diabetes (T2DM) risk have also been identified, but how they do so remains enigmatic. Nevertheless, defective insulin secretion emerges as the main culprit in both monogenic and polygenic diabetes, with environmental and lifestyle factors, via obesity, accounting for the current dramatic increase in T2DM. There also have been significant advances in therapy, particularly for some monogenic disorders. We review here what ails the beta cell and how its function may be restored.
引用
收藏
页码:1160 / 1171
页数:12
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