Importance of [beta]-Catenin in glucose and energy homeostasis

In settings of increased insulin demand, failure to expand pancreatic β-cells mass leads to diabetes. Genome-wide scans of diabetic populations have uncovered several genes associated with susceptibility to type 2 diabetes and a number of them are part of the Wnt signaling. β-Catenin, a Wnt downstre...

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Bibliographic Details
Published in:Scientific reports 2012-09, Vol.2, p.693
Main Authors: Elghazi, Lynda, Gould, Aaron P, Weiss, Aaron J, Barker, Daniel J, Callaghan, John, Opland, Darren, Myers, Martin, Cras-méneur, Corentin, Bernal-mizrachi, Ernesto
Format: Article
Language:English
Subjects:
Clonal deletion
Cre recombinase
Diabetes
Diabetes mellitus
Ectopic expression
Energy balance
Energy expenditure
Energy metabolism
Genomes
Glucose tolerance
High fat diet
Homeostasis
Hyperactivity
Hypothalamus
Insulin
Pancreas
Wnt protein
β-Catenin
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Summary:In settings of increased insulin demand, failure to expand pancreatic β-cells mass leads to diabetes. Genome-wide scans of diabetic populations have uncovered several genes associated with susceptibility to type 2 diabetes and a number of them are part of the Wnt signaling. β-Catenin, a Wnt downstream effector participates in pancreatic development, however, little is known about its action in mature β-cells. Deletion of β-Catenin in Pdx1 pancreatic progenitors leads to a decreased β-cell mass and impaired glucose tolerance. Surprisingly, loss of β-catenin made these mice resistant to high fat diet because of their increased energy expenditure and insulin sensitivity due to hyperactivity. The complexity of this phenotype was also explained in part by ectopic expression of Cre recombinase in the hypothalamus. Our data implicates β-Catenin in the regulation of metabolism and energy homeostasis and suggest that Wnt signaling modulates the susceptibility to diabetes by acting on different tissues.
ISSN:2045-2322
DOI:10.1038/srep00693