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Effect of Maternal Zinc Deficiency or Food Restriction on Rat Fetal Pancreas. I. Procarboxypeptidase A and Chymotrypsinogen1

Leann K. Robinson and Lucille S. Hurley2

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

Maternal zinc deficiency lowered the protein, zinc and zymogen content of the day 19 rat fetal pancreas. Pregnant Sprague-Dawley rats were fed a zinc-deficient diet (0.4 ± 0.1 ppm zinc) ad libitum or a zinc-supplemented control diet (100 ppm zinc) either ad libitum or with restricted intake. At day 19 of pregnancy, the pancreata from zinc-deficient fetuses contained 50% less zinc and 15% less cellular protein than did fetal pancreas from normal or restricted intake controls, although DNA content was normal. Zymogen granulation of pancreatic acinar cells from zinc-deficient fetuses was decreased. The two major proteolytic zymogens of the rat fetal pancreas—procarboxypeptidase A, a zinc metalloprotein, and chymotrypsinogen—were each 30% lower per cell in zinc-deficient fetuses than in controls. Zinc-deficient fetuses taken from large litters of seven or more young per litter had lower levels of procarboxypeptidase A and chymotrypsinogen in the pancreata than did fetuses taken from smaller litters. The results suggest that exocrine zymogen accumulation is lower than normal in the pancreata of zinc-deficient fetuses, irrespective of the zinc dependency of the enzyme proteins involved.


KEY WORDS: • pancreatic development • zinc deficiency • procarboxypeptidase A • chymotrypsinogen

1 Supported in part by NIH grant HD-01743 from the National Institute of Child Health and Human Development. L. Robinson was a Procter and Gamble Predoctoral Fellow.

2 To whom reprint requests should be sent.

Manuscript received 9 July 1980.





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