Secretory state regulates Zn<sup>2+</sup> transport in gastric parietal cell of the rabbit

Naik, Haley B.; Beshire, Melissa; Walsh, Breda M.; Liu, Jingjing; Soybel, David I.

doi:10.1152/ajpcell.00577.2008

Cited by 13 publications

(28 citation statements)

References 45 publications

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“…In the stomach, this may be needed to meet increased requirements for Zn-dependent proteins during lactation such as gastrin [24] [25], perhaps driven by increased expression of Zip11 [26, 27]. Alternatively, Zn is physiologically coupled to acid secretion [28] which is consistent with increased stomach acid secretion during lactation [29]. Consistent with the need to increase the digestion, absorption and assimilation of nutrients, we show for the first time that pancreatic Zn concentration increases by ~50% during lactation.…”

Section: Discussionmentioning

confidence: 99%

Redistribution of tissue zinc pools during lactation and dyshomeostasis during marginal zinc deficiency in mice

McCormick

King²,

Krebs

et al. 2015

Journal of Trace Elements in Medicine and Biology

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Zinc (Zn) requirements are increased during lactation. Increased demand is partially met through increased Zn absorption from the diet. It is estimated that 60 to 80% of women of reproductive age are at risk for Zn deficiency due to low intake of bioavailable Zn and increased demands during pregnancy and lactation. How Zn is redistributed within the body to meet the demands of lactation, and how Zn deficiency affects this process, is not understood. Female C57bl/6J mice were fed a control (ZA; 30 mg Zn/kg) or a marginally Zn deficient (ZD; 15 mg Zn/kg) diet for 30 d prior to mating through mid-lactation and compared with nulliparous mice fed the same diets. While stomach and plasma Zn concentration increased during lactation in mice fed ZA, mice fed ZD had lower stomach Zn concentration and abrogated plasma Zn levels during lactation. Additionally, femur Zn decreased during lactation in mice fed ZA, while mice fed ZD did not experience this decrease. Furthermore, red blood cell, pancreas, muscle and mammary gland Zn concentration increased, and liver and adrenal gland Zn decreased during lactation, independent of diet, while kidney Zn concentration increased only in mice fed ZD. Finally, maternal Zn deficiency significantly increased the liver Zn concentration in offspring but decreased weight gain and survival. This study provides novel insight into how Zn is redistributed to meet the increased metabolic demands of lactation and how marginal Zn deficiency interferes with these homeostatic adjustments.

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Section: Discussionmentioning

confidence: 99%

Redistribution of tissue zinc pools during lactation and dyshomeostasis during marginal zinc deficiency in mice

McCormick

King²,

Krebs

et al. 2015

Journal of Trace Elements in Medicine and Biology

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“…Chronic Zn 2+ deficiency is well recognized as a risk factor for infection and poor healing. Increasingly, however, it has become clear that demand of peripheral tissues and parenchymal cells for Zn 2+ may occur in response to endocrine stimulation (45), normal physiologic activity (46), as well as oxidative stress (47,48) and systemic sepsis (24). Rapidly deployable assays for free Zn 2+ in extracellular fluids such as the one described here are crucial for development of studies to understand how such acute demand for Zn 2+ is satisfied and to identify experimental conditions and clinical circumstances in which the capacity of the circulation to deliver Zn 2+ is insufficient to meet the demand.…”

Section: Discussionmentioning

confidence: 99%

Redistribution of labile plasma zinc during mild surgical stress in the rat

Kelly

Mathew

Kohler

et al. 2011

Translational Research

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Zinc is an essential trace element and co-factor for many cellular processes. Uptake of Zn 2+ in peripheral tissues depends on its total content in the circulation, and on mechanisms facilitating delivery to tissues in its labile form. Understanding mechanisms of Zn 2+ delivery has been hindered by the absence of techniques to detect labile Zn 2+ in the circulation. In this study, we report the use of the fluorescent zinc-binding dye, ZnAF-2, to detect changes in labile Zn 2+ in the circulating plasma of the rat under standardized conditions, including exogenous infusions to raise plasma Zn 2+ , and infusion of the chelator, citrate, to lower labile Zn 2+ in the plasma without altering total Zn2+ content. In a model of mild surgical stress (unilateral femoral arterial ligation), plasma levels of total and labile Zn 2+ decreased significantly 24 hours following operation. Ultrafiltration of plasma into high and low molecular weight macromolecule fractionations indicated that binding capacity of zinc in the high molecular weight fraction is impaired for the entire 24 hour interval following induction of mild surgical stress. Affinity of the filtrate fraction was rapidly and reversibly responsive to anesthesia alone, decreasing significantly at 4 hours and recovering at 24 hours; in animals subjected to moderate surgical stress this responsiveness was lost. These are the first reported measurements of labile Zn 2+ in the circulation in any form of mild systemic stress. Zinc undergoes substantial redistribution in the plasma, response to surgical stress, leading to increased availability in lower molecular weight fractions and in its labile form.

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“…Following transfer to glass coverslips and equilibration in standard Ringer's solutions, fluorescence imaging of individual glands was performed as described previously [18]. Glands loaded with fluozin-3AM were excited at 488 nm with emission measurement at 520 nm.…”

Section: Methodsmentioning

confidence: 99%

“…In gastric mucosa, adequate intracellular stores and luminal content of Zn 2+ may regulate integrity of [19] and acid secretion by [18], [22] the gastric glands and enhance protection of the mucosa as a whole against acid-peptic injury [23], [24]. Little is known, however, of the content and distribution of Zn 2+ within the mucosa, or of the mechanisms that regulate the flow of Zn 2+ into the parietal cell during secretory stimulation.…”

Section: Introductionmentioning

confidence: 99%

Demand for Zn2+ in Acid-Secreting Gastric Mucosa and Its Requirement for Intracellular Ca2+

et al. 2011

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Background and AimsRecent work has suggested that Zn2+ plays a critical role in regulating acidity within the secretory compartments of isolated gastric glands. Here, we investigate the content, distribution and demand for Zn2+ in gastric mucosa under baseline conditions and its regulation during secretory stimulation.Methods and FindingsContent and distribution of zinc were evaluated in sections of whole gastric mucosa using X-ray fluorescence microscopy. Significant stores of Zn2+ were identified in neural elements of the muscularis, glandular areas enriched in parietal cells, and apical regions of the surface epithelium. In in vivo studies, extraction of the low abundance isotope, 70Zn2+, from the circulation was demonstrated in samples of mucosal tissue 24 hours or 72 hours after infusion (250 µg/kg). In in vitro studies, uptake of 70Zn2+ from media was demonstrated in isolated rabbit gastric glands following exposure to concentrations as low as 10 nM. In additional studies, demand of individual gastric parietal cells for Zn2+ was monitored using the fluorescent zinc reporter, fluozin-3, by measuring increases in free intracellular concentrations of Zn2+ {[Zn2+]i} during exposure to standard extracellular concentrations of Zn2+ (10 µM) for standard intervals of time. Under resting conditions, demand for extracellular Zn2+ increased with exposure to secretagogues (forskolin, carbachol/histamine) and under conditions associated with increased intracellular Ca2+ {[Ca2+]i}. Uptake of Zn2+ was abolished following removal of extracellular Ca2+ or depletion of intracellular Ca2+ stores, suggesting that demand for extracellular Zn2+ increases and depends on influx of extracellular Ca2+.ConclusionsThis study is the first to characterize the content and distribution of Zn2+ in an organ of the gastrointestinal tract. Our findings offer the novel interpretation, that Ca2+ integrates basolateral demand for Zn2+ with stimulation of secretion of HCl into the lumen of the gastric gland. Similar connections may be detectable in other secretory cells and tissues.

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Secretory state regulates Zn²⁺ transport in gastric parietal cell of the rabbit

Abstract: Naik HB, Beshire M, Walsh BM, Liu J, Soybel DI. Secretory state regulates Zn 2ϩ transport in gastric parietal cell of the rabbit.

Cited by 13 publications

References 45 publications

Redistribution of tissue zinc pools during lactation and dyshomeostasis during marginal zinc deficiency in mice

Redistribution of tissue zinc pools during lactation and dyshomeostasis during marginal zinc deficiency in mice

Redistribution of labile plasma zinc during mild surgical stress in the rat

Demand for Zn2+ in Acid-Secreting Gastric Mucosa and Its Requirement for Intracellular Ca2+

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Secretory state regulates Zn2+ transport in gastric parietal cell of the rabbit

Abstract: Naik HB, Beshire M, Walsh BM, Liu J, Soybel DI. Secretory state regulates Zn 2ϩ transport in gastric parietal cell of the rabbit.

Cited by 13 publications

References 45 publications

Redistribution of tissue zinc pools during lactation and dyshomeostasis during marginal zinc deficiency in mice

Redistribution of tissue zinc pools during lactation and dyshomeostasis during marginal zinc deficiency in mice

Redistribution of labile plasma zinc during mild surgical stress in the rat

Demand for Zn2+ in Acid-Secreting Gastric Mucosa and Its Requirement for Intracellular Ca2+

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Secretory state regulates Zn²⁺ transport in gastric parietal cell of the rabbit