Journal
CELL
Volume 148, Issue 6, Pages 1160-1171Publisher
CELL PRESS
DOI: 10.1016/j.cell.2012.02.010
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Funding
- Wellcome Trust
- MRC
- Royal Society
- Diabetes UK
- Medical Research Council [G0801995] Funding Source: researchfish
- Wellcome Trust [095531/Z/11/Z] Funding Source: researchfish
- MRC [G0801995] Funding Source: UKRI
- Wellcome Trust [095531/Z/11/Z] Funding Source: Wellcome Trust
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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.
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