Journal
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
Volume 310, Issue 5, Pages R459-R468Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpregu.00439.2015
Keywords
zinc deficiency; Zip4 processing; small intestine; alkaline phosphatase; glucose homeostasis
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Funding
- Japan Society for the Promotion of Science [26660086, 15H04501, 23248020]
- Fuji Foundation for Protein Research
- Central Miso Research Institute
- Skylark Food Science Institute
- Iijima Memorial Foundation for the Promotion of Food Science and Technology
- Japan Food Chemical Research Foundation
- All Japan Coffee Association
- Asahi Group Foundation
- Mitsui Sumitomo Insurance Welfare Foundation
- Yamazaki Spice Promotion Foundation
- Food Science Institute Foundation
- Grants-in-Aid for Scientific Research [14J06743, 15K14728, 26660086, 15H04501, 23248020] Funding Source: KAKEN
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Systemic and cellular zinc homeostasis is elaborately controlled by ZIP and ZnT zinc transporters. Therefore, detailed characterization of their expression properties is of importance. Of these transporter proteins, Zip4 functions as the primarily important transporter to control systemic zinc homeostasis because of its indispensable function of zinc absorption in the small intestine. In this study, we closely investigated Zip4 protein accumulation in the rat small intestine in response to zinc status using an anti-Zip4 monoclonal antibody that we generated and contrasted this with the zinc-responsive activity of the membrane-bound alkaline phosphatase (ALP). We found that Zip4 accumulation is more rapid in response to zinc deficiency than previously thought. Accumulation increased in the jejunum as early as 1 day following a zinc-deficient diet. In the small intestine, Zip4 protein expression was higher in the jejunum than in the duodenum and was accompanied by reduction of ALP activity, suggesting that the jejunum can become zinc deficient more easily. Furthermore, by monitoring Zip4 accumulation levels and ALP activity in the duodenum and jejunum, we reasserted that zinc deficiency during lactation may transiently alter plasma glucose levels in the offspring in a sex-specific manner, without affecting homeostatic control of zinc metabolism. This confirms that zinc nutrition during lactation is extremely important for the health of the offspring. These results reveal that rapid Zip4 accumulation provides a significant conceptual advance in understanding the molecular basis of systemic zinc homeostatic control, and that properties of Zip4 protein accumulation are useful to evaluate zinc status closely.
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