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Physiol. Genomics 3: 17-23, 2000;
1094-8341/00 $5.00
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Received 28 February 2000; accepted in final form 11 May 2000.
Physiological Genomics 3:17-23 (2000)
1094-8341/00 $5.00 © 2000 American Physiological Society

Diet effects on weight gain and body composition in high growth (hg/hg) mice

PABLO M. CORVA and JUAN F. MEDRANO

Department of Animal Science, University of California, Davis, California 95616-8521

Corva, Pablo M., and Juan F. Medrano. Diet effects on weight gain and body composition in high growth (hg/hg) mice. Physiol Genomics 3: 17–23, 2000.—Nongenetic factors such as nutrition modulate the effects of genes responsible for overgrowth in animals. The goal of this study was to examine the importance of genotype x diet interactions on the effects of a major locus that regulates growth in the mouse. We have examined the phenotype of high growth (hg), a partially recessive autosomal locus that increases growth rate and mature body size. C57BL/6J (C57) and congenic C57BL/6J-hg/hg (HG) mice were fed three experimental diets differing in protein and energy content from 3 to 12 wk of age. HG mice grew faster and were, on average, 51% heavier than C57 at 12 wk of age. Feed intake was higher in HG mice but proportional to the increase in body weight. The magnitude of the differences in body size and composition between lines depended on the interaction between genotype and the protein/energy ratio of the diet. In C57, the diets modified the level of fatness without changing adult lean mass. However, in HG the diets differentially affected both linear growth and body composition. In general, HG had higher plasma levels of insulin-like growth factor I at 3 and 12 wk than C57. Plasma insulin did not differ between lines, but leptin was higher for C57 mice fed a high-energy diet. These results show that the effects of hg on growth are modulated by diet composition. Therefore, this mutation could be a valuable model with which to study the genetic and nutritional aspects of overgrowth disorders.

genetics; overgrowth; genotype-nutrition interactions; insulin-like growth factor I; leptin




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