Subnormal albumin gene expression is associated with weight loss in immunodeficient/DNA-repair-deficient wasted mice

摘要

Mice bearing the autosomal recessive mutation wst express a disease syndrome of immunodeficiency, neurologic dysfunction, and increased sensitivity to the killing effects of ionizing radiation. The mice were originally characterized as ''wasted'' because of their dramatic weight loss that begins at 21 days of age and progresses until death at 28-32 days of age. Because of the reported association between abnormal liver status and weight loss, we examined expression of a variety of liver-specific genes in wst/wst 10 mice relative to littermate (wst/(center dot)) and parental strain (BCF(sub 1)) controls. Interestingly, the results revealed a greater than 67% reduction in albumin mRNA expression in livers derived from wst/wst mice relative to both controls. Expression of alpha-fetoprotein as well as a variety of other liver-specific genes (secretory component, metallothionein, cytochrome P(sub 1)450, transferrin receptor, tumor necrosis factor, and Ia antigen) was unaffected. These results suggest a relationship between low albumin expression and wasting syndromes in mice. In addition, we believe that our data suggest the wasted mouse as a unique model for subnormal albumin expression in humans.