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J. Biol. Chem., Vol. 282, Issue 51, 37053-37063, December 21, 2007

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Znt7 (Slc30a7)-deficient Mice Display Reduced Body Zinc Status and Body Fat Accumulation^*

Liping Huang^¶1, Yan Yiu Yu, Catherine P. Kirschke, Erik R. Gertz, and Kent K. C. Lloyd^||

From the United States Department of Agriculture/Agriculture Research Service/Western Human Nutrition Research Center, Department of Nutrition, ^||Center for Comparative Medicine, ^¶Rowe Program in Genetics, University of California, Davis, California 95616

In vitro studies have demonstrated that ZNT7 is involved in transporting the cytoplasmic zinc into the Golgi apparatus of the cell for zinc storage or to be incorporated into newly synthesized zinc-requiring enzymes/proteins. To evaluate the physiological role of ZNT7, we created a mouse model of Znt7 deficiency by a gene-trap approach. Znt7-deficient mice were zinc-deficient based on their low zinc content in serum, liver, bone, kidney, and small intestine. In embryonic fibroblasts isolated from Znt7-deficient mice, cellular zinc was 50% that of wild-type controls. Znt7-deficient mice also displayed some classic manifestations of dietary zinc deficiency, such as reduced food intake and poor body weight gain. However, the mutant mice did not show any sign of hair abnormality and dermatitis that are commonly associated with dietary zinc deficiency. A radioactive feeding study suggested that Znt7-deficient mice had reduced zinc absorption in the gut resulting in decreased zinc accumulations in other organs in the body. The poor growth found in Znt7-deficient mice could not be corrected by feeding the mutant mice with a diet containing 6-fold higher zinc (180 mg/kg) than the suggested adequate intake amount (30 mg/kg). Furthermore, the reduced body weight gain of the mutant mice was largely due to the decrease in body fat accumulation. We conclude that ZNT7 has essential functions in dietary zinc absorption and in regulation of body adiposity.

Received for publication, August 9, 2007 , and in revised form, October 12, 2007.

^* This work was supported by United States Dept. of Agriculture Grants CRIS: 5306-53000-008-00D and CRIS:5306-515-30-014-00D. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence should be addressed: United States Department of Agriculture/Agriculture Research Service/Western Human Nutrition Research Center, 430 West Health Sciences Drive, University of California, Davis, CA 95616. Tel.: 530-754-5756; Fax: 530-752-5295; E-mail: liping.huang{at}ars.usda.gov.

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