Dietary calcium deficiency increases Ca2+ uptake and Ca2+ extrusion mechanisms in chick enterocytes

Centeno, Viviana; Barboza, Gabriela E. Díaz de; Marchionatti, Ana Maria Estivalete; Alisio, Arturo; Dallorso, M. E.; Nasif, Renée; Talamoni, Nori G. Tolosa de

doi:10.1016/j.cbpb.2004.08.002

Cited by 52 publications

(54 citation statements)

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“…A relationship with the process of fat absorption (4) and preservation of the normal homeostasis of the gut microbiota has been described previously (5) . IAP expression parallels that of other intestinal proteins involved in Ca absorption under vitamin D stimulation: Ca channel TRPV6, calbindin CD 9k , calcium sodium exchanger NCX 1 and Ca pump PMCAb1 (3,6,7) . Experiments carried out in vitro with purified IAP from the intestine of rats have demonstrated an interaction between Ca and IAP (8) .…”

mentioning

confidence: 79%

“…The amount of Ca in food and faeces was determined by atomic absorption spectroscopy (Arolab MK II, Buenos Aires, Argentina), and 24 h Ca intake and 24 h faecal Ca were calculated. The %Ca for each animal was calculated as %Ca ¼ (24 h Ca intake 2 24 h faecal Ca) £ 100/24 h Ca intake, on day 1 (%Ca 1 ) and on day 3 (%Ca 3 ).…”

Section: In Vivo Calcium Absorptionmentioning

confidence: 99%

“…The effect of Phe on Ca absorption was analysed by the comparison of %Ca 1 -(in the absence of Phe) and %Ca 3 -(in the presence of Phe) for each group with different amounts of Ca in the diet. Day 2 was not included in the analyses because Ca in the faeces is a mixture of the period with and without Phe.…”

Section: In Vivo Calcium Absorptionmentioning

confidence: 99%

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Luminal calcium concentration controls intestinal calcium absorption by modification of intestinal alkaline phosphatase activity

2011

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Intestinal alkaline phosphatase (IAP) is a brush-border phosphomonoesterase. Its location suggests an involvement in the uptake of nutrients, but its role has not yet been defined. IAP expression parallels that of other proteins involved in Ca absorption under vitamin D stimulation. Experiments carried out in vitro with purified IAP have demonstrated an interaction between Ca and IAP. The gut is prepared to face different levels of Ca intake over time, but high Ca intake in a situation of a low-Ca diet over time would cause excessive entry of Ca into the enterocytes. The presence of a mechanism to block Ca entry and to avoid possible adverse effects is thus predictable. Thus, in the present study, Sprague -Dawley rats were fed with different amounts of Ca in the diet (0·2, 1 and 2 g%), and the percentage of Ca absorption (%Ca) in the presence and absence of L-phenylalanine (Phe) was calculated. The presence of Phe caused a significant increase in %Ca (52·3 (SEM 6·5) % in the presence of Phe v. 31·1 (SEM 8·9) % in the absence of Phe, regardless of the amount of Ca intake; paired t test, P¼ 0·02). When data were analysed with respect to Ca intake, a significant difference was found only in the group with low Ca intake (paired t test, P¼0·03). Additionally, IAP activity increased significantly (ANOVA, P,0·05) as Ca concentrations increased in the duodenal lumen. The present study provides in vivo evidence that luminal Ca concentration increases the activity of IAP and simultaneously decreases %Ca, acting as a minute-to-minute regulatory mechanism of Ca entry.

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confidence: 79%

Section: In Vivo Calcium Absorptionmentioning

confidence: 99%

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Luminal calcium concentration controls intestinal calcium absorption by modification of intestinal alkaline phosphatase activity

2011

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“…Serum Ca 2þ levels may be normal or low, according to the extent and degree of Ca 2þ deficiency. We have demonstrated hypocalcaemia in chicks after 10 d of low Ca 2þ intake (0·1%) (16,17) . The mechanisms of adaptation to low-Ca 2þ diets depend on the vitamin D status, mainly of the rate of 1,25-dihydroxyvitamin D 3 (1,25(OH) 2 D 3 ) synthesis.…”

Section: Introductionmentioning

confidence: 99%

Molecular mechanisms triggered by low-calcium diets

et al. 2009

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Ca is not only essential for bone mineralisation, but also for regulation of extracellular and intracellular processes. When the Ca2+ intake is low, the efficiency of intestinal Ca2+ absorption and renal Ca2+ reabsorption is increased. This adaptive mechanism involves calcitriol enhancement via parathyroid hormone stimulation. Bone is also highly affected. Low Ca2+ intake is considered a risk factor for osteoporosis. Patients with renal lithiasis may be at higher risk of recurrence of stone formation when they have low Ca2+ intake. The role of dietary Ca2+ on the regulation of lipid metabolism and lipogenic genes in adipocytes might explain an inverse relationship between dairy intake and BMI. Dietary Ca2+ restriction produces impairment of the adipocyte apoptosis and dysregulation of glucocorticosteroid metabolism in the adipose tissue. An inverse relationship between hypertension and a low-Ca2+ diet has been described. Ca2+ facilitates weight loss and stimulates insulin sensitivity, which contributes to the decrease in the blood pressure. There is also evidence that dietary Ca2+ is associated with colorectal cancer. Dietary Ca2+ could alter the ratio of faecal bile acids, reducing the cytotoxicity of faecal water, or it could activate Ca2+-sensing receptors, triggering intracellular signalling pathways. Also it could bind luminal antigens, transporting them into mucosal mononuclear cells as a mechanism of immunosurveillance and promotion of tolerance. Data relative to nutritional Ca2+ and incidences of other human cancers are controversial. Health professionals should be aware of these nutritional complications and reinforce the dairy intakes to ensure the recommended Ca2+ requirements and prevent diseases.

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“…Low Ca 2+ diets increase the intestinal Ca 2+ absorption ratio, at least in part, by altering the vitamin D endocrine system [9, 10] and the lipid composition and fluidity of intestinal membranes [11]. …”

Section: Introductionmentioning

confidence: 99%

Minireview on Regulation of Intestinal Calcium Absorption

Pérez¹,

Picotto²,

Carpentieri

et al. 2008

Digestion

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An overview of current information on the mechanisms by which intestinal calcium absorption occurs is described in this article. Both paracellular and transcellular pathways are analyzed. Special emphasis focuses on molecules participating in the latter pathway, such as TRPV5 and TRPV6 channels, located in the apical region of the enterocytes, CB_9k and CB_28k, presumably involved in the cation movement from the apical to the basolateral pole of the cell, and PMCA_1b and Na⁺/Ca²⁺ exchanger, proteins that extrude Ca²⁺ from the cells. Current concepts on the relative importance of paracellular and transcellular calcium transport and the vitamin D dependence of each pathway are referred and analyzed showing the contrasting views on this issue. More detailed information is given regarding the stimulatory effect of vitamin D on intestinal Ca²⁺ absorption either in animal models or in the human intestine. The possible mechanisms triggered by hormones such as PTH, calcitonin, estrogen, thyroid hormone, glucocorticoids and different nutritional factors on intestinal calcium absorption are also reviewed. Finally, the influence of physiological conditions such as growth, pregnancy, lactation and aging on intestinal calcium absorption are discussed.

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Dietary calcium deficiency increases Ca2+ uptake and Ca2+ extrusion mechanisms in chick enterocytes

Cited by 52 publications

References 36 publications

Luminal calcium concentration controls intestinal calcium absorption by modification of intestinal alkaline phosphatase activity

Luminal calcium concentration controls intestinal calcium absorption by modification of intestinal alkaline phosphatase activity

Molecular mechanisms triggered by low-calcium diets

Minireview on Regulation of Intestinal Calcium Absorption

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