Novel mechanisms controlling insulin release and fat deposition ...(naling in pancreatic beta-cells was redu...),Health

Date:5/13/2008

naling in pancreatic beta-cells was reduced by the actions of the growth factor Activin B through the ALK7 receptor, and that blood glucose levels regulates the expression of both Activin B and ALK7. In agreement with these results, mice lacking Activin B also developed hyperinsulinemia to a similar extent as ALK7 mutants.

In other words, our data revealed an unexpected negative feedback loop in the control of glucose-dependent insulin release, mediated the actions of Activin B on the ALK7 receptor, says Carlos Ibez.

In the second study, the scientists found that mice lacking ALK7 accumulated less fat and gained less weight than their normal counterparts when fed on a high-fat diet. They discovered that another growth factor called GDF3 could also signal via the ALK7 receptor, and that mice lacking GDF3 showed similar defects in fat deposition and weight gain as the ALK7 mutants. Intriguingly, however, mutant mice consumed equal amounts of food as their normal counterparts during the experiment.

These results show that lack of ALK7 or GDF3 improves energy balance in the body under regimes of high caloric intake, says Carlos Ibez.

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Contact: Katarina Sternudd katarina.sternudd@ki.se 46-852-483-895 Karolinska Institutet Source:Eurekalert

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