作者: T. Doi , C. Pesce , Chih-Wei Yang , G. E. Striker , S. Elliot
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摘要: BACKGROUND Mice transgenic for bovine growth hormone (bGH) gene have increased body weight and severe glomerulosclerosis leading to death in uremia. EXPERIMENTAL DESIGN The aim of this study was determine if were mediated by different bGH regions. Amino acid substitutions the alpha-helix III generated, lines mice that expressed these products developed. Female carrying native (bGH mice), a mutated encodes destabilized (bGH-L121P, E126G; bGH-m11 or perfect amphiphilic (bGH-E117L, G119R, A122D; bGH-m8 mice) examined at 2-3 months 6-9 age. Body, kidney, heart weights measured. Urinary glucose, albumin, creatinine, serum glucose measured all mice. Serum levels insulin-like factor I (IGF-I) month group. Whole blood hemoglobin A1 some Kidney sections light immunofluorescence microscopy. Glomerular volume related allometry. RESULTS developed indistinguishable from seen mice, even though they had normal size. exceeded allometry both strains. glomeruli appropriate size histologic appearance; however, dwarfs. IGF-I mice; also an albumin/creatinine ratio months. None hyperglycemic. CONCLUSIONS These data indicated development promotion regions molecule. glomerular response unique consisted glomerulosclerosis.