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The Effect of Varying Dietary Zinc Levels on the Concentration and Localization of Zinc in Rat Bile-Pancreatic Fluid^1,2,

Department of Nutrition, University of California, Davis, CA 95616

To determine if zinc homeostasis occurs by zinc output from bile-pancreatic secretions, the bile-pancreatic duct and intestine of rats were surgically cannulated, and bile-pancreatic fluid was collected 2 h/d from the day of surgery to 8 d after surgery. The rats were fed diets containing 10, 100 or 1000 µg Zn/g diet before and after surgery. The effect of surgery itself was significant; food intake was initially lower than presurgery levels, but returned to presurgery levels by d 5. Protein and zinc concentrations, and carboxypeptidase A (CpA) and carboxypeptidase B (CpB) activities in bile-pancreatic fluid increased after surgery and leveled off at approximately d 6. Among the dietary zinc groups, the concentration of zinc in bile-pancreatic fluid varied significantly, whereas concentrations of calcium and copper did not. Zinc concentration in bile-pancreatic fluid for d 1–8 postsurgery averaged 1.8, 3.2 and 4.4 µg Zn/g, in the groups fed 10, 100 and 1000 µg Zn/g diet, respectively. Because the percent of zinc ingested that was secreted in bile-pancreatic fluid, estimated to be 57, 9.5 and 1.2% for the groups consuming the diets containing 10, 100 and 1000 µg Zn/g diet respectively, was not similar in the three groups, the quantity of zinc in bile-pancreatic fluid is not proportionally related to the amount of zinc ingested. Our results therefore suggest that zinc secretion in bile-pancreatic fluid does not play a major role in zinc homeostasis. Molecular localization of zinc in bile-pancreatic fluid and measurement of activity of CpA and CpB indicated that zinc in bile-pancreatic fluid is associated primarily with these digestive enzymes.

KEY WORDS: • zinc • zinc homeostasis • bile • pancreatic fluid • molecular localization

¹ Presented in part at the Annual Meeting of the Federation of Societies for Experimental Biology, St. Louis, MO, April 13–18, 1986.

² Supported in part by National Institutes of Health Research Grant No. HD-01743 from the National Institute of Child Health and Human Development.

³ Present address: Food Science and Nutrition Department, California Polytechnic State University, San Luis Obispo, CA 93407.

⁴ To whom correspondence should be sent.

Manuscript received 21 March 1986. Revision accepted 26 February 1987.