Journal
DIABETES
Volume 63, Issue 4, Pages 1283-1288Publisher
AMER DIABETES ASSOC
DOI: 10.2337/db13-1435
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Funding
- National Institutes of Health (NIH) [U01-DK-089529, R01-DK-088383]
- NIH/National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) [U01-DK-070430]
- Beckman Research Center/NIDDK/Integrated Islet Distribution Program [10028044]
- NIH [U42-RR0-06042]
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The recent discovery of betatrophin, a protein secreted by the liver and white adipose tissue in conditions of insulin resistance and shown to dramatically stimulate replication of mouse insulin-producing beta-cells, has raised high hopes for the rapid development of a novel therapeutic approach for the treatment of diabetes. At present, however, the effects of betatrophin on human beta-cells are not known. Here we use administration of the insulin receptor antagonist S961, shown to increase betatrophin gene expression and stimulate beta-cell replication in mice, to test its effect on human beta-cells. Although mouse beta-cells, in their normal location in the pancreas or when transplanted under the kidney capsule, respond with a dramatic increase in beta-cell DNA replication, human beta-cells are completely unresponsive. These results put into question whether betatrophin can be developed as a therapeutic approach for treating human diabetes.
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