Journal
MAMMALIAN GENOME
Volume 17, Issue 11, Pages 1065-1077Publisher
SPRINGER
DOI: 10.1007/s00335-006-0054-2
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Funding
- NIAAA NIH HHS [R01AA12715, R01AA011028] Funding Source: Medline
- NIDCD NIH HHS [R01DC00882] Funding Source: Medline
- NIDDK NIH HHS [R01 DK094759, R01DK046791, R01 DK046791-12, R01DK 058797, R01 DK058797, R01 DK046791] Funding Source: Medline
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To understand how genotype influences fat patterning and obesity, we conducted an autosomal genome scan using male and female F-2 hybrids between the C57BL/6ByJ and 129P3/J parental mouse strains. Mice were studied in middle-adulthood and were fed a low-energy, low-fat diet during their lifetime. We measured the weight of the retroperitoneal adipose depot (near the kidney) and the gonadal adipose depot (near the epididymis in males and ovaries in females). An important feature of the analysis was the comparison of linkage results for absolute adipose depot weight and depot weight adjusted for body size, i.e., relative weight. We detected 67 suggestive linkages for six phenotypes, which fell into one of three categories: those specific to absolute but not relative depot weight (Chr 5, 11, and 14), those specific to relative but not absolute depot weight (Chr 9, 15, and 16), and those involving both (Chr 2 and 7). Some quantitative trait loci (QTLs) affected one adipose depot more than another: Retroperitoneal depot weight was linked to Chr 8, 11, 12, and 17, but the linkage effects for the gonadal depot were stronger for Chr 5, 7, and 9. Several linkages were specific to sex; for instance, the absolute weight of gonadal fat was linked to Chromosome 7 in male (LOD = 3.4) but not female mice (LOD = 0.2). Refining obesity as a phenotype may uncover clues about gene function that will assist in positional cloning efforts.
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