期刊
PANCREATOLOGY
卷 10, 期 4, 页码 467-476出版社
ELSEVIER SCIENCE BV
DOI: 10.1159/000266284
关键词
Carboxyl-ester lipase; MODY; Exocrine dysfunction
资金
- Haukeland University Hospital
- Innovest
- Research Council of Norway
- University of Bergen, Norway
- Fulbright Foundation
- ESPE
- Norwegian Research Council
- Manpei Suzuki Diabetes Foundation, Japan
- JDRF
- National Institutes of Health [DK33201, DK55545]
- Joslin Diabetes and Endocrinology Research Center [5P30 DK36836]
- Joslin Diabetes Center [DK34834, RO1 DK 67536]
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK036836, R01DK033201, R01DK055545, R01DK067536] Funding Source: NIH RePORTER
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, alpha- and beta-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. Copyright (C) 2010 S. Karger AG, Basel and IAP
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据