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Title:   Author  item
                                            Huang, Lipingitem
                                            YU, YAN YIU - UCD NUTR. DEPT.item
                                            Kirschke, Catherineitem
                                            Gertz, Erikitem
                                            KENT K.C., LLOYD - UCD, COMPARATIVE MEDICINE
  Submitted to: Journal of Biological Chemistry
                                    Publication Type: Peer Reviewed Journal
                                    Publication Acceptance Date: 10/12/2007
                                    Publication  Date: 12/21/2007
                                    Citation: Huang, L., Yu, Y., Kirschke, C.P., Gertz, E.R., Kent K.C., L. 2008.   Znt7 (Slc30a7)-Deficient Mice Display Rreduced Body ZincC Status and Body Fat Accumulation. Journal of Biological Chemistry. 282,51:37053-37063, 2007.Interpretive Summary: In vitro studies have demonstrated that ZNT7 is involved in transporting zinc from the cytoplasm (the internal fluid of the cell) into the Golgi apparatus (an organelle in the cytoplasm in which proteins synthesized by the cell are processed and packaged) for zinc storage or to be incorporated into the 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 contents in serum, liver, bone, kidney, and small intestine. In embryonic fibroblasts isolated from Znt7-deficient mice, cellular zinc was about 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 (65Zn) feeding study suggested that Znt7-deficient mice had a reduced zinc absorption in the gut resulting in a decreased zinc accumulation 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.
                                Technical Abstract: 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 the 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 contents in serum, liver, bone, kidney, and small intestine. In embryonic fibroblasts isolated from Znt7-deficient mice, cellular zinc was about 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 a reduced zinc absorption in the gut resulting in a decreased zinc accumulation 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.


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