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Pancreatology. 2010;10(4):467-76. doi: 10.1159/000266284. Epub 2010 Aug 19.

Pancreatic function in carboxyl-ester lipase knockout mice.

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  • 1Department of Pediatrics, Haukeland University Hospital, Bergen, Norway.

Abstract

BACKGROUND/AIMS:

CEL-MODY is a monogenic form of diabetes and exocrine pancreatic insufficiency due to mutations in the carboxyl-ester lipase (CEL) gene. We aimed to investigate endocrine and exocrine pancreatic function in CEL knockout mice (CELKO).

METHODS:

A knockout mouse model with global targeted deletion of CEL was investigated physiologically and histopathologically, and compared to littermate control CEL+/+ mice at 7 and 12 months on normal chow and high-fat diets (HFD), i.e. 42 and 60% fat by calories.

RESULTS:

CELKO+/+ and -/- mice showed normal growth and development and normal glucose metabolism on a chow diet. Female CEL-/- mice on 60% HFD, on the other hand, had increased random blood glucose compared to littermate controls (p = 0.02), and this was accompanied by a reduction in glucose tolerance that did not reach statistical significance. In these mice there was also islet hyperplasia, however, α- and β-islet cells appeared morphologically normal and pancreatic exocrine function was also normal.

CONCLUSION:

Although we observed mild glucose intolerance in female mice with whole-body knockout of CEL, the full phenotype of human CEL-MODY was not reproduced, suggesting that the pathogenic mechanisms involved are more complex than a simple loss of CEL function. and IAP.

Copyright © 2010 S. Karger AG, Basel.

PMID:
20720448
[PubMed - indexed for MEDLINE]
PMCID:
PMC2968766
Free PMC Article
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