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• W2182306574 endingPage "R990" @default.
• W2182306574 startingPage "R985" @default.
• W2182306574 abstract "In an effort to understand the genetics of human obesity, we have studied the physiology and molecular genetics of rodent models with monogenetic forms of obesity including the leptin gene-defective ( Lep ob / Lep ob ) and leptin receptor gene-defective ( Lepr db / Lepr db ) mouse. In the experiments reported here, we investigated the effects of heterozygosity at Lep ob and Lepr db on body composition and circulating leptin concentration in +/+, Lepr db /+, and Lep ob /+ adult mice to identify possible gene dosage effects of these mutations that might elucidate their physiology. Adult mice heterozygous for the Lep ob or Lepr db allele had equivalent fat mass and percentage body fat, which was increased 27–47% and 23–35%, respectively, relative to +/+ littermates. Plasma leptin concentrations adjusted for fat mass were 6.5 ng/ml in the Lep ob /+, 9.6 ng/ml in the +/+, and 11.5 ng/ml in the Lepr db /+ mice. Sex had no effect on plasma leptin after controlling for fat mass. These data, and data from a small number of mice heterozygous at both Lep ob and Lepr db (compound heterozygotes), suggest that leptin protein produced per mass of body fat is reduced in Lep ob /+ mice and that body fat is increased in Lep ob /+ mice until plasma leptin concentrations reach that of a normal +/+ mouse. The elevated plasma leptin concentration in the Lepr db /+ mice suggests that LEPR may mediate autocrine suppression of Lep expression. These results raise the possibility that human mutations that have even subtle effects on the leptin/leptin receptor system in either the homozygous or heterozygous state may have significant effects on adiposity." @default.
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• W2182306574 date "1998-04-01" @default.
• W2182306574 modified "2023-09-26" @default.
• W2182306574 title "Heterozygosity for<i>Lep^ob</i>or<i>Lepr^db</i>affects body composition and leptin homeostasis in adult mice" @default.
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• W2182306574 doi "https://doi.org/10.1152/ajpregu.1998.274.4.r985" @default.
• W2182306574 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9575960" @default.
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