Genetics and physiology of dietary obesity in the mouse.
1996
West D.B. | York B. | Goudey Lefevre J. | Truett G.E.
AKR/J and SWR/J inbred mice differ markedly in their sensitivity to dietary obesity. Male AKR/J mice increase adiposity approximately threefold, whereas SWR/J remain relatively lean when fed a high-fat diet for twelve weeks. At 5 weeks of age these mouse strains have comparable body fat percentages when fed a low-fat diet, yet they differ in a number of metabolic markers. AKR/J mice are less physically active, have a higher rate of excretion of norepinephrine in the urine, have increased sensitivity to insulin-stimulated glucose disposal and decreased maximally stimulated epinephrine lipolysis in isolated adipocytes. These metabolic markers may represent underlying physiological differences under genetic control, which partially explain the differential sensitivity to dietary obesity in these two strains. A quantitative analysis of the segregation of body adiposity in F2 and F1 X SWR/J progeny suggests that this phenotype is under the control of a minimum of three to four genes and that there is partial dominance of the AKR/J genotype. Molecular mapping in F2 and F1 X SWR/J populations using the quantitative trait loci mapping approach and random simple sequence length polymorphisms has identified several quantitative trait loci with significant likelihood of of-the-odds scores that are linked to dietary obesity. These loci are located on chromosomes 4, 9, and 15, and several candidate genes are co-localized at these loci.
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