Physiological consequences of ectopic agouti gene expression:: the yellow obese mouse syndrome

被引:104
作者
Wolff, GL
Roberts, DW
Mountjoy, KG
机构
[1] US FDA, Div Biochem Toxicol, Natl Ctr Toxicol Res, Jefferson, AR 72079 USA
[2] Univ Arkansas Med Sci, Dept Biochem Mol Biol, Little Rock, AR 72205 USA
[3] Univ Arkansas Med Sci, Dept Pharmacol Interdisciplinary Toxicol, Little Rock, AR 72205 USA
[4] Univ Auckland, Res Ctr Dev Med & Biol, Auckland 1, New Zealand
[5] Univ Auckland, Dept Mol Med, Auckland 1, New Zealand
关键词
background genome; melanocortin; pseudoagouti mice; response to environmental stimuli; tumorigenesis;
D O I
10.1152/physiolgenomics.1999.1.3.151
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
This review summarizes primary and downstream phenotypic manifestations, with emphasis on altered responsiveness to environmental stimuli, of dominant yellow mutations at the mouse agouti locus. Obvious effects include hyperinsulinemia, obesity, stimulation of somatic growth and tumorigenesis, and coat color. Downstream influences of hyperinsulinemia and obesity on the individual's physiology determine important components of the obese yellow agouti mouse syndrome. Collectively, the phenotypic aberrations described support the concept that identical genomes are expressed in a spectrum of physiological phenotypes that reflect the complex interdependence of gene-regulated physiological pathways and processes in the organism throughout extended, but temporally ordered, periods of fetal and neonatal development and aging. This summary identifies important areas for additional research and provides integrated information required for a systematic approach to the development of interventions for common adult human health problems.
引用
收藏
页码:151 / 163
页数:13
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