Pancreatic Metallothionein-I May Play a Role in Zinc Homeostasis during Maternal Dietary Zinc Deficiency in Mice
| Autor: | Dae Kee Lee, Jodi Dufner-Beattie, Jim Geiser, Glen K. Andrews |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Genetically modified mouse
medicine.medical_specialty Genotype Transgene Medicine (miscellaneous) chemistry.chemical_element Mice Transgenic Zinc Biology Mice Pregnancy Internal medicine medicine Animals Homeostasis Metallothionein Yolk sac Pancreatic elastase Nutrition and Dietetics Pancrelipase medicine.disease Diet medicine.anatomical_structure Endocrinology chemistry Zinc deficiency Female Pancreas |
| Zdroj: | The Journal of Nutrition. 133:45-50 |
| ISSN: | 0022-3166 |
| DOI: | 10.1093/jn/133.1.45 |
| Popis: | Herein, the function of pancreatic metallothionein (MT)-I during zinc deficiency in pregnancy was examined using transgenic mice, which constitutively express the mouse MT-I gene driven by the rat elastase I promoter. Pancreatic MT protein levels and zinc levels were elevated significantly in the transgenic mice compared with those in control mice. Pregnant transgenic and control mice were fed zinc-deficient (1 micro g/g beginning at d 8) or zinc-adequate (50 micro g/g) diets during pregnancy, and the effects on the morphology of embryos were determined at d 14 of pregnancy (d 1 = vaginal plug). As other indicators of zinc deficiency, maternal pancreatic MT levels, as well as the expression of zinc-regulated genes in the embryonic visceral yolk sac were examined. Under these experimental conditions of moderate dietary zinc deficiency, 21.3% of the embryos in control mice exhibited morphological defects, whereas only 5.8% of the embryos in the elastase-MT-I transgenic females had developed abnormally by d 14. Surprisingly, dietary zinc deficiency caused a >95% decrease in pancreatic MT protein concentration in these transgenic mice. This suggests the post-transcriptional control of MT protein levels during zinc deficiency because the rat elastase I promoter is not metal-regulated. The decrease in pancreatic MT protein levels was paralleled by a dramatic decrease in the relative abundance of MT-I mRNA and a dramatic increase in the relative abundance of the zinc/iron regulated transporter-related zinc transporter-4 (ZIP4) mRNA in the embryonic visceral yolk sac. Thus, the constitutive overexpression of pancreatic MT-I in these mice attenuated, but did not prevent the effects of maternal or embryonic zinc deficiency under these conditions. Overall, these findings are consistent with the hypothesis that mouse pancreatic MT-I may participate in providing a labile pool of maternal zinc for the developing embryo during periods of zinc deficiency. |
| Databáze: | OpenAIRE |
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