Aluminum effects upon calbindin D9k-linked duodenal calcium transport in diabetic male rats

Orihuela, Daniel; Favre, Cristián; Monti, Juan A.; Carnovale, Cristina E.; Carrillo, Marı́a C.

doi:10.1016/s0378-4274(98)00367-1

Cited by 5 publications

(6 citation statements)

References 27 publications

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“…This result demonstrates for the first time that aluminum intake can inhibit gene expression in vivo and supports the hypothesis that aluminum interferes with the biological actions of vitamin D in the intestine. These conclusions are consistent with studies demonstrating that aluminum inhibits vitamin D-dependent calcium absorption in experimental animals (20,(22)(23)(24)28). Whether physiological functions in other tissues expressing calbindin-D28k, such as the kidney, bone or pancreatic ␤ cells (29), are also affected by aluminum at the level of mRNA expression is not known.…”

Section: Discussionsupporting

confidence: 88%

“…Aluminum could have inhibited expression by causing reductions in serum levels of 1,25(OH) 2 D because previous studies have indicated that aluminum may decrease renal conversion of vitamin D to 1,25(OH) 2 D (23). In that study and others, however, it was also shown that aluminum inhibits the ability of physiological injections of 1,25(OH) 2 D to increase calbindin concentrations in the intestine (11,20,23). Therefore, aluminum inhibited calbindin expression even in the presence of physiological levels of the active hormone.…”

Section: Discussionmentioning

confidence: 75%

“…Low calcium diets are a physiologic stimulus to increase circulating levels of 1,25(OH) 2 D, enhance calbindin gene expression and, in cooperation with other vitamin D-dependent processes, increase the efficiency of calcium absorption (17,21). Consistent with these inhibitory effects of aluminum on intestinal calbindin levels, studies have shown that aluminum inhibits the ability of vitamin D to increase the efficiency of intestinal calcium absorption in experimental animals (20,(22)(23)(24).…”

mentioning

confidence: 93%

“…Its concentration is also thought to be regulated at both transcriptional and posttranscriptional levels by 1,25(OH) 2 D, in cooperation with other regulatory factors (18,19). In both rats and chicks, aluminum toxicity inhibits the classic ability of injected 1,25(OH) 2 D to upregulate the concentration of intestinal calbindin (11,20). In a more practical setting, we have shown that dietary aluminum also inhibits the upregulation of intestinal calbindin when chicks are placed on a low calcium diet (10).…”

mentioning

confidence: 99%

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Aluminum Toxicity Alters the Regulation of Calbindin-D28k Protein and mRNA Expression in Chick Intestine

Cox

Dunn

2001

The Journal of Nutrition

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Previous studies have shown that aluminum inhibits vitamin D-dependent calcium absorption. The mechanism involves reduced sensitivity to 1,25-dihydroxycholecalciferol and reduced expression of the calcium transport protein, calbindin-D28k. Reduced expression of calbindin protein may be due to decreased levels of calbindin mRNA. To test this hypothesis, we measured calbindin mRNA levels in chicks fed diets with and without added aluminum. Groups of chicks were fed one of four diets: control, control plus aluminum, low calcium, or low calcium plus aluminum. A fifth group was fed a vitamin D-free diet as a negative control. Calbindin protein was measured by immunoblotting. Serum calcium and inorganic phosphorus were determined. Intestinal mRNA was isolated and assayed by slot-blot hybridization to a fluorescein-conjugated oligonucleotide probe complementary to calbindin-D28k mRNA. Antifluorescein antibodies conjugated to alkaline phosphatase were used to detect hybrids and mRNA levels were quantified by densitometry. Specificity of the probe was verified by Northern analysis. Intestinal calbindin protein was greater in the control plus aluminum group than in controls, but no difference in calbindin mRNA was observed. These changes were associated with small decreases in serum phosphorus and calcium, suggesting a postranscriptional effect of aluminum. Chicks fed the low calcium diet had greater intestinal calbindin protein and mRNA levels relative to the control group in association with a 45% decrease in serum calcium. In contrast, no difference in calbindin protein, and significantly less mRNA were found in the low calcium plus aluminum group compared with controls, despite a decrease in serum calcium similar to that of chicks fed the low calcium diet without aluminum. These results show that in chicks fed a low calcium diet, aluminum intake decreases transcription and/or stability of intestinal calbindin mRNA, and that aluminum may inhibit the expression of vitamin D-dependent genes. J. Nutr. 131: 2007Nutr. 131: -2013Nutr. 131: , 2001.Aluminum can accumulate in the body whenever uptake exceeds the disposal of this metal via urinary or biliary excretion (1). Toxic accumulation most often occurs from large oral intakes, contaminated parenteral solutions or in individuals with renal insufficiency. Aluminum toxicity has been clearly demonstrated in patients with renal failure (2). It has also been reported in preterm infants fed intravenously (3), healthy premature infants (4), healthy adults chronically consuming aluminum containing antacids and their offspring (5,6).The symptoms of aluminum toxicity include neurodegenerative disorders, mycrocytic anemia unresponsive to iron and bone disease (vitamin D-resistant osteomalasia). The molecular mechanisms causing these symptoms are not well understood. Many biochemical processes have been shown to be affected by aluminum, but there is little agreement as to which are relevant to its toxic effects. Some proposed mechanisms include disrupting membrane function,...

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 75%

mentioning

confidence: 93%

mentioning

confidence: 99%

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Aluminum Toxicity Alters the Regulation of Calbindin-D28k Protein and mRNA Expression in Chick Intestine

Cox

Dunn

2001

The Journal of Nutrition

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“…Nevertheless, data showing that the oral administration of aluminum produces a diminution in calcium excretion have been reported (Sanchez et al 1997). Al has an inhibiting effect on the Ca intestinal transport that is dependent on vitamin D through an effect on the calbindina D (Adler et al 1989;Dunn et al 1995, Orihuela et al 1999). …”

Section: Discussionmentioning

confidence: 99%

Effects of aluminum on phosphate metabolism in rats: a possible interaction with vitamin D3 renal production

et al. 2004

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The effect of chronic aluminum (Al) administration on the phosphorous (Pi) metabolism of different target tissues was studied. Male Wistar rats received aluminum lactate for 3 months (5.75 mg/kg bodyweight of Al, i.p., three times per week). The animals were studied at the end of the 1st, 2nd and 3rd month of treatment. They were housed individually in metabolic cages for 4 days to study Pi and calcium (Ca) balance. Daily food and water intakes were recorded for all animals and urine and feces were collected for Pi and calcium assays. After 3 months the Pi intestinal absorption and the Pi deposition in bone were studied using 32Pi. Another group of rats was treated daily for 7 days with calcitriol (0.08 microg/kg body weight in sesame oil, i.p.) and the Pi balance was studied for the last 4 days. The results indicated that chronic administration of Al affected simultaneously the Pi and calcium balance, with a significant diminution of calcium and increased Pi accretion in bones, together with a diminution in the intestinal absorption of Pi. The treatment of the rats with calcitriol promoted a normalized Pi balance in Al treated rats. These findings suggest that Al could modify the Pi metabolism acting directly on intestine, kidney and bone, or indirectly through possible changes in the levels of vitamin D3.

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Aggravated dyslipidemia in diabetic albino rats after subchronic oral aluminium chloride exposure

Igwenagu,

Egbe-Nwiyi,

Igbokwe

2024

Comp Clin Pathol

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Aluminum effects upon calbindin D9k-linked duodenal calcium transport in diabetic male rats

Cited by 5 publications

References 27 publications

Aluminum Toxicity Alters the Regulation of Calbindin-D28k Protein and mRNA Expression in Chick Intestine

Aluminum Toxicity Alters the Regulation of Calbindin-D28k Protein and mRNA Expression in Chick Intestine

Effects of aluminum on phosphate metabolism in rats: a possible interaction with vitamin D3 renal production

Aggravated dyslipidemia in diabetic albino rats after subchronic oral aluminium chloride exposure

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