Journal
NATURE COMMUNICATIONS
Volume 5, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms6308
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Funding
- Marie Curie International Re-Integration Grant [PIRG07-GA-2010-268397]
- Foreningen framjorande Diabetes Forskning (FFDF)
- KI stiftelse
- Karolinska Institutet
- Swedish Research Council
- Novo Nordisk Foundation
- Swedish Diabetes Association
- Family Knut and Alice Wallenberg Foundation
- Diabetes Research and Wellness Foundation
- Berth von Kantzow's Foundation
- Skandia Insurance Company, Ltd
- Strategic Research Programme in Diabetes at Karolinska Institutet [ERC-2013-AdG 338936-BetaImage]
- Stichting af Jochnick Foundation
- Family Erling-Persson Foundation
- MRC [G0801843] Funding Source: UKRI
- Medical Research Council [G0801843] Funding Source: researchfish
- Novo Nordisk Fonden [NNF12OC1016557] Funding Source: researchfish
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Type 2 diabetes mellitus is affecting more than 382 million people worldwide. Although much progress has been made, a comprehensive understanding of the underlying disease mechanism is still lacking. Here we report a role for the beta-cell primary cilium in type 2 diabetes susceptibility. We find impaired glucose handling in young Bbs4(-/-) mice before the onset of obesity. Basal body/ciliary perturbation in murine pancreatic islets leads to impaired first phase insulin release ex and in vivo. Insulin receptor is recruited to the cilium of stimulated beta-cells and ciliary/basal body integrity is required for activation of downstream targets of insulin signalling. We also observe a reduction in the number of ciliated beta-cells along with misregulated ciliary/basal body gene expression in pancreatic islets in a diabetic rat model. We suggest that ciliary function is implicated in insulin secretion and insulin signalling in the beta-cell and that ciliary dysfunction could contribute to type 2 diabetes susceptibility.
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