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This version published online on April 1, 2004
Endocrinology, doi:10.1210/en.2004-0219
A more recent version of this article appeared on July 1, 2004
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Submitted on February 18, 2004
Accepted on March 25, 2004

Genetic background (C57BL/6J versus FVB/N) strongly influences the severity of diabetes and insulin resistance in ob/ob mice

Martin Haluzik*, Carlo Colombo, Oksana Gavrilova, Streamson Chua, Nicole Wolf, Min Chen, Bethel Stannard, Kelly R. Dietz, Derek Le Roith, and Marc L. Reitman

Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892; 3 Department of Medicine, 1 Faculty of Medicine, Charles University, Prague, Czech Republic; Division of Molecular Genetics and New York Obesity Research Center, Department of Pediatrics, Columbia University, New York, NY 10032; Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892

* To whom correspondence should be addressed. E-mail: mhalu{at}lf1.cuni.cz.

We studied the effects of genetic background on the phenotype of ob/ob mice, a model of severe obesity, insulin resistance and diabetes caused by leptin deficiency. Despite comparable degree of obesity and hyperinsulinemia, C57BL/6J ob/ob mice had much milder hyperglycemia and, surprisingly, normal circulating adiponectin levels despite still prominent signs of insulin resistance. Hyperinsulinemic-euglycemic clamp revealed relatively less whole body and muscle insulin resistance in C57BL/6J ob/ob mice, while liver insulin resistance tended to be more severe than in FVB/N ob/ob mice. C57BL/6J ob/ob mice had also more rapid clearance of circulating triglycerides and more severe hepatic steatosis. We suggest that strain related distinction in lipid handling is the most important player in the differences in diabetic phenotype and insulin sensitivity, while the impact of circulating adiponectin levels on the overall phenotype of ob/ob mice is less important.
Key words: obesity • diabetes • insulin resistance • genetic background • adiponectin • resistin • glucose clamp • mouse • glucose uptake • liver steatosis




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