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Disruption of beta cell acetyl-CoA carboxylase-1 in mice impairs insulin secretion and beta cell mass – published online 17/10/2018

Fig from Cantley paper

James Cantley, Aimee Davenport, Laurène Vetterli, Nandor J. Nemes, P. Tess Whitworth, Ebru Boslem, Le May Thai, Natalie Mellett, Peter J. Meikle, Kyle L. Hoehn, David E. James, Trevor J. Biden

The role of glucose oxidation in triggering insulin secretion from pancreatic beta cells is well characterised. Glucose also drives anaplerotic flux, leading to the production of malonyl-CoA by the enzyme acetyl-CoA carboxylase 1 (ACC1), yet the role of ACC1 in beta cell function in vivo is not clear. In this issue, using tissue-specific ACC1 gene (Acaca) knockout mouse models and a combination of in vivo and ex vivo experiments, Cantley et al ( report that beta cell ACC1 activity is necessary for normal insulin secretion profiles and whole body glucose homeostasis. Moreover, they reveal that long-term loss of beta cell ACC1 leads to reductions in beta cell size and levels of enzymes involved in protein synthesis. These results demonstrate the importance of the ACC1-coupled pathway in sustaining adequate beta cell growth and function and suggest that potential strategies to enhance this pathway could promote a functional beta cell mass during diabetes.

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