Gallbladder Glycoprotein Secretion in Mice With Hemolytic Anemia and Pigment Gallstones

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Abstract
The nb/nb mouse with hereditary hemolytic anemia provides an animal model for the study of pigment gallstone disease. We measured glycoprotein synthesis and secretion in gallbladder neck and fundus of 6–month–old mice without stones, and in 12–month–old mice with and without stones in order to determine the effect of age and presence or absence of stones on mucin release. We observed that the gallbladder necks of 12–month–old nb/nb mice with pigment stones secreted more 3H–glucosamine–labeled glycoprotein (68.2 dpm per m¨g protein) than did the gallbladder necks of mice without pigment stones (31.1 dpm per m¨g protein). When expressed as a percentage of total glycoprotein synthesis in the gallbladder neck, secretion of glycoprotein was 23.4% in 6–month–old hemolytic mice and 28.7% in 12–month–old hemolytic mice without pigment stones. However, in the presence of pigment stones, the percentage of secreted glycoprotein rose to 40.8%, which differed significantly from both 6–month–old (p < 0.02) and 12–month–old mice without stones (p < 0.05). Our results suggest that the presence of gallstones in nb/ nb mice was associated with a localized increase in glycoprotein release from gallbladder neck. The mechanism for this increase may be precipitation of pigment–mucin concretions in the gallbladder neck glands which has been previously described in this animal model.