Journal
CELL METABOLISM
Volume 27, Issue 3, Pages 549-+Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2018.01.015
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Funding
- Diabetes Research Institute Foundation (DRIF)
- American Diabetes Association Innovative grant [1-17-ICTS-052, R21DK114418]
- Swedish Diabetes Association
- Swedish Research Council
- Novo Nordisk Foundation
- Family Erling-Persson Foundation
- Strategic Research Program in Diabetes at Karolinska Institutet
- ERC-AdG [338936-BetaImage]
- ERC-PoC [727306]
- Family Knut and Alice Wallenberg Foundation
- Skandia Insurance Company Ltd
- Diabetes and Wellness Foundation
- Bert von Kantzow Foundation
- Stichting af Jochnick Foundation
- NIH [F32DK083226, K01DK097194, R01DK084321, R56DK084321, R01DK111538, R01DK113093, R21ES025673]
- European Research Council (ERC) [727306] Funding Source: European Research Council (ERC)
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Every animal species has a signature blood glucose level or glycemic set point. These set points are different, and the normal glycemic levels (normoglycemia) of one species would be life threatening for other species. Mouse normoglycemia can be considered diabetic for humans. The biological determinants of the glycemic set point remain unclear. Here we show that the pancreatic islet imposes its glycemic set point on the organism, making it the bona fide glucostat in the body. Moreover, and in contrast to rodent islets, glucagon input from the alpha cell to the insulin-secreting beta cell is necessary to fine-tune the distinctive human set point. These findings affect transplantation and regenerative approaches to treat diabetes because restoring normoglycemia may require more than replacing only the beta cells. Furthermore, therapeutic strategies using glucagon receptor antagonists as hypoglycemic agents need to be reassessed, as they may reset the overall glucostat in the organism.
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