Retention of zinc and calcium from the human colon

Sandström, B; Cederblad, Åke; Kivistö, Barbro; Stenquist, Bo; Andersson, H

doi:10.1093/ajcn/44.4.501

Cited by 50 publications

(31 citation statements)

References 15 publications

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“…Subsequently, the absorption of free, short chain fatty acids will be met with a much more rapid response mediated by the exchanger. Since zinc is not hydrolyzed and only 10% of dietary zinc is absorbed (19), this ion is present at high concentrations along the entire digestive tract (19,20,39) and is thus ideally suited for a signaling role there.…”

Section: Discussionmentioning

confidence: 99%

“…This was reduced by ϳ30% at higher zinc concentrations (200 M). The results of this analysis show that zinc at concentrations found in the digestive tract (19,20,39), which induce Ca 2ϩ release through the ZnR (13), also trigger phosphorylation of ERK1/2.…”

Section: Specificity and Temporal Dependence Of Erk1/2mentioning

confidence: 95%

“…Importantly, the Ca 2ϩ response induced by the ZnR in HT29 cells is triggered by ϳ80 M zinc, i.e. within the physiological range of zinc concentrations found in the digestive tract (19,20). Interestingly, activation of the ZnR also resulted in activation of Na ϩ /H ϩ exchange in colonocytes.…”

mentioning

confidence: 89%

“…We therefore used zinc in Ringer's solution, such that the free zinc concentrations obtained (calculated using Geochem software, Ref. 13) are similar to those present in the digestive tract (19,20). Phosphorylation of ERK1/2 was monitored in cells exposed to the indicated concentrations of free zinc for 10 min (Fig.…”

Section: Specificity and Temporal Dependence Of Erk1/2mentioning

confidence: 99%

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Extracellular Zinc Triggers ERK-dependent Activation of Na+/H+ Exchange in Colonocytes Mediated by the Zinc-sensing Receptor

Azriel-Tamir

Sharir²,

Schwartz

et al. 2004

Journal of Biological Chemistry

120

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Extracellular zinc promotes cell proliferation and its deficiency leads to impairment of this process, which is particularly important in epithelial cells. We have recently characterized a zinc-sensing receptor (ZnR) linking extracellular zinc to intracellular release of calcium. In the present study, we addressed the role of extracellular zinc, acting via the ZnR, in regulating the MAP kinase pathway and Na Arrested cell proliferation is a hallmark of zinc deficiency. This is particularly true in gastrointestinal cells (1-4), where insufficient dietary zinc attenuates the renewal of the epithelium leading to severe diarrhea (1). Extracellular zinc has been shown to regulate cell proliferation via the MAP 1 kinase pathway in several cell types (5-7). Although the mitogenic and anti-apoptotic effects of zinc are well recognized (8, 9), and the treatment of severe diarrhea by addition of dietary zinc is common, the direct link between this ion and the cellular mechanisms regulating proliferation is not well understood. It has been suggested that a decrease in intracellular zinc may lead directly to a reduction in activity of various metalloenzymes involved in transcription and cell metabolism (1, 10). Several studies, however, indicate that extracellular zinc acts as a signaling molecule. In tracheal cells, for example, extracellular zinc, through activation of Src, leads to transactivation of EGFR and subsequently to activation of ERK1/2 (11). In fibroblasts, extracellular zinc has been shown to trigger the activation of the PI3K pathway, subsequently leading to the activation of AKT and the S6 kinase (12). The signaling pathways linking extracellular zinc to these proteins and to subsequent regulation of cellular ion, pH or volume homeostasis, however, remain poorly understood.We have recently identified and characterized an extracellular zinc-sensing receptor (ZnR) that triggers, upon exposure to extracellular zinc, the release of Ca 2ϩ from intracellular stores by activation of the IP 3 pathway (13). The pharmacological profile of the calcium response triggered by the ZnR, particularly its sensitivity to the PLC inhibitor, U73122, and the inhibitory effect of the IP 3 receptor blocker, 2-APB, indicates that the ZnR is a G q -coupled receptor (GPCR). Both the G␣ and the G␤␥ dimer of various GPCRs have been linked to activation of the MAP kinase via multiple intracellular pathways (14 -16). In intestinal cells, furthermore, the muscarinic receptor has been shown to play a key role in promoting ion transport through activation of MAP and PI 3-kinase signal transduction (17,18). A role for the ZnR in activation of the MAP kinase pathway is demonstrated in this work.The ZnR was initially characterized in the colonocytic cell line, HT29, where a robust calcium signal was generated following activation of the receptor by changes in the concentration of extracellular Zn 2ϩ (13). Importantly, the Ca 2ϩ response induced by the ZnR in HT29 cells is triggered by ϳ80 M zinc, i.e. within the physiological range of zinc conc...

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Section: Discussionmentioning

confidence: 99%

Section: Specificity and Temporal Dependence Of Erk1/2mentioning

confidence: 95%

mentioning

confidence: 89%

Section: Specificity and Temporal Dependence Of Erk1/2mentioning

confidence: 99%

See 2 more Smart Citations

Extracellular Zinc Triggers ERK-dependent Activation of Na+/H+ Exchange in Colonocytes Mediated by the Zinc-sensing Receptor

Azriel-Tamir

Sharir²,

Schwartz

et al. 2004

Journal of Biological Chemistry

120

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“…Reports on the relative contribution of the different sections of the intestine vary, and it has been suggested that the major site of absorption might shift with differences in food matrix and body Zn status. Absorption can occur throughout the total length of the small intestine, but colonic absorption is limited (Sandstrom et al 1986). Fractional Zn absorption falls with increasing dose (Istfan et al 1983), but increases fairly rapidly in response to reductions in dietary Zn intake (Wada et al 1985).…”

Section: S U S a N J Fairweather-taitmentioning

confidence: 99%

Zinc in Human Nutrition

Fairweather‐Tait

1988

Nutr. Res. Rev.

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Differences in Serum Zn Levels in Acutely Ill and Recovered Adolescents and Young Adults with Anorexia Nervosa – A Pilot Study

Zepf

Sungurtekin

Glass

et al. 2011

Euro Eating Disorders Rev

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Preliminary evidence suggests that changes in zinc (Zn) metabolism are associated with anorexia nervosa (AN). However, data are scarce regarding potential differences in serum Zn concentrations in adolescent and young adult patients with AN. It was the aim of the present pilot study to compare serum Zn concentrations between acutely ill and remitted adolescent and young adult female patients with AN and female controls. Zn concentrations were higher in remitted compared with acutely ill patients. Zn concentrations were also higher in remitted patients compared with controls, but there was no significant difference in Zn concentrations between acutely ill patients and controls. The present study provides preliminary evidence for differences in serum Zn status in recovered patients with AN. These differences are likely influenced by reported food preferences, in particular as regards Ca²⁺ and phosphorus-containing foods. However, because of limited statistical power, future research involving larger samples is necessary.

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Retention of zinc and calcium from the human colon

Cited by 50 publications

References 15 publications

Extracellular Zinc Triggers ERK-dependent Activation of Na+/H+ Exchange in Colonocytes Mediated by the Zinc-sensing Receptor

Extracellular Zinc Triggers ERK-dependent Activation of Na+/H+ Exchange in Colonocytes Mediated by the Zinc-sensing Receptor

Zinc in Human Nutrition

Differences in Serum Zn Levels in Acutely Ill and Recovered Adolescents and Young Adults with Anorexia Nervosa – A Pilot Study

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