| First Author | Beamer WG | Year | 1982 |
| Journal | Mouse News Lett | Volume | 67 |
| Pages | 21 | Mgi Jnum | J:13923 |
| Mgi Id | MGI:62101 | Citation | Beamer WG, et al. (1982) [Adipose storage deficiency (asd)]. Mouse News Lett 67:21 |
| abstractText | Full text of MNL contribution: 3. Adipose storage deficiency (asd) A new autosomal recessive mutation with subtle dwarfing characterized by shortness of tail, limbs, body length, and nose, arose in the C57BL/6By strain. Mutant males are reproductively sterile for reasons independent of gonadal and reproductive tract morphology or of sperm numbers, morphology, and motility. Approximately one-half of the mutant females will produce one or more litters; however, offspring must be fostered because of inadequate lactation. Mutants tend to die between 150-200 days of age from undetermined causes. Skeletal studies show that mutant bones are significantly shorter but thicker than those of normal sibs. Mineral ash content of various bones is identical for mutant and normal littermates. Serum calcium and phosphorus levels are normal. Thus, linear bone growth is reduced without alteration of mineralization. Mutant mice are essentially devoid of visually identifiable adipose tissue except for brown fat. Body composition analyses confirmed the deficiency of adipose tissue in that mutant mice (weighing 15% less than normal littermates) had 38, 60, and 72% less total fat at 1, 3, and 5 months than found in normal littermates. Serum cholesterol is significantly less in mutant than in normal littermates, while blood sugar, liver glycogen, plasma insulin, and serum thyroxine levels are normal. Free fatty acids are synthesized from normal precursors; however, the storage of fatty acids only occurs in liver triglycerides Thus, the mutant gene appears to affect adipocytes in an undetermined fashion and therefore has been given the provisional name and gene symbol of adipose storage deficiency (asd). (W. G. Beamer and D. L. Coleman) |
