1 Introduction: 26RFa (QRFP) is a biologically active peptide that has been found to control 2 feeding behaviour by stimulating food intake, and to regulate glucose homeostasis by acting as 3 an incretin. The aim of the present study was thus to investigate the impact of 26RFa gene 4 knockout on the regulation of energy and glucose metabolism. 5Research design and methods: 26RFa mutant mice were generated by homologous 6 recombination, in which the entire coding region of prepro-26RFa was replaced by the iCre 7 sequence. Energy and glucose metabolism was evaluated through measurement of 8 complementary parameters. Morphological and physiological alterations of the pancreatic islets 9 were also investigated. 10Results: Our data do not reveal significant alteration of energy metabolism in the 26RFa-11 deficient mice except the occurrence of an increased basal metabolic rate. By contrast, 26RFa 12 mutant mice exhibit an altered glycemic phenotype with an increased hyperglycemia after a 13 glucose challenge associated with an impaired insulin production, and an elevated hepatic 14 glucose production. 2D and 3D immunohistochemical experiments indicate that the insulin 15 content of pancreatic β cells is much lower in the 26RFa -/mice as compared to the wild-type 16 littermates. 17Conclusion: Disruption of the 26RFa gene induces substantial alteration in the regulation of 18 glucose homeostasis with, in particular, a deficit in insulin production by the pancreatic islets. 19These findings further support the notion that 26RFa is an important regulator of glucose 20 homeostasis. 21 22
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