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Everyone needs to maintain his or her blood glucose levels within a narrow physiological range, neither too high nor too low. Defects in this regulation can lead to serious conditions such as diabetes. This carefully maintained balance, or homeostasis, relies on two hormones: insulin and glucagon. Therefore, it is essential to understand how levels of glucose are regulated. New insights into how this glucose homeostasis is achieved are uncovered in a report to be published in the April issue of Nature Cell Biology.
In the pancreas, there are two types of cells that respond to the hormones regulating glucose levels: Beta-cells, which produce insulin in response to rising levels of blood glucose, and alpha-cells, which produce glucagon in response to low glucose levels. The activity of insulin leads to a decrease in blood sugar levels, whereas the activity of glucagon raises blood sugar levels. How beta-cells respond to high glucose levels and secrete insulin has been widely studied, but only now does new work from Dr Claes Wollheim and colleagues from the University Medical Center, Geneva, report how alpha-cells respond to changes in glucose levels. Wolheim and colleagues show that, surprisingly, alpha-cells secrete glucagons in response to a glucose intermediate. In conditions of high glucose levels beta-cells act to inhibit this response of alpha-cells. This suppression appears to involve zinc released from the beta-cells. To ensure the two cell types of the pancreas respond differently to the same signal, the beta-cells appear to repress the secretion of glucagon from alpha-cells. Further work to dissect how zinc is released from beta-cells and how it represses glucagon secretion from alpha-cells is likely to provide new avenues for the treatment of diabetes. Author contact:
Claes Wollheim
Department of Internal Medicine
University Medical Center
Geneva, Switzerland
Tel: +41 22 702 5548
Email: claes.wollheim@medicine.unige.ch Also available online. (C) Nature Cell Biology press release.
Message posted by: Trevor M. D'Souza
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