Effects of diabetes on cecal and colonic calcium transport in the rat.

Petith, M. Michael; Schedl, Harold P.

doi:10.1152/ajpendo.1978.235.6.e699

Cited by 10 publications

(5 citation statements)

References 15 publications

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“…In agree ment with these findings, diabetic rats de velop a negative calcium balance [3] and greatly depressed vitamin D-dependent [4][5][6][7] duodenal calcium-binding protein and cal cium transport [3], We have found a vitamin D-dependent calcium-binding protein in ce cum and colon, which appears to be identical with that of the duodenum [8]. Since diabetes is associated with depression of calcium transport by the large intestine [9], we exam ined the effects of streptozotocin diabetes on calcium-binding protein of cecum and colon and report our results.…”

supporting

confidence: 59%

“…Cecal and colonic CaBP are also vitamin D dependent [8]. Dia betic rats show other evidence for vitamin D deficiency including decreased duodenal [3,15,16] and cecal and colonic [9] calcium transport in comparison with controls. The depression of calcium transport in diabetes is also the result of deficiency of l,25-(OH)2D since the transport defect is corrected by ad ministration of l,25-(OH)2D [17], and by in sulin treatment [16], which restores 1,25-(OH)2D to normal in diabetes [1], Based on our previous study of vitamin D metabolites in diabetes [1], the present study shows that CaBP of cecum and colon re sponds to lower levels of serum 1,25-dihydroxyvitamin D in the diabetic state.…”

Section: Discussionmentioning

confidence: 99%

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Effects of Diabetes on Calcium-Binding Protein in the Cecum and Colon of the Rat

1981

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Calcium-binding protein (CaBP) was measured in the mucosa of cecum and colon of pair-fed control and diabetic rats. After extraction from mucosa, CaBP was purified by Bio-gel P-100 chromatography, and eluted fractions were analyzed by Chelex assay to define the peak of CaBP. Total CaBP content of mucosa in cecum was slightly depressed in diabetics compared to controls, but was decreased to one-third the control value in colon. Specific activity (CaBP per g mucosa and per mg protein) of diabetics was reduced to two-thirds the control value in both segments. Thus, in diabetes, the response of large intestinal CaBP is similar, but of lower magnitude than that of duodenum.

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supporting

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Effects of Diabetes on Calcium-Binding Protein in the Cecum and Colon of the Rat

1981

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“…In short-term (5 -12 days) experimental dia¬ betic rats, Schneider et al (1974) have also similarly reported increased serum PTH levels. Factors such as intestinal calcium malabsorption, hypercalciuria, and increased faecal calcium excretion have been considered to be the causes of the negative calcium balance in these rats (Schneider & Schedi 1972;Schneider et al 1976Schneider et al , 1977Petith & Schedi 1978). Furthermore, the present study has clearly shown that the decreased calcium, 25(OH)D, and 24,25(OH)2D concentra¬ tions in STZ diabetic rats are completely normal¬ ized by insulin treatment and are accompanied by an improvement of metabolic disorders such as liver dysfunction and accelerated catabolism.…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, it has been shown that hypercalciuria in diabetic patients is ameliorated with insulin therapy (Raskin et al 1978). Furthermore, intestinal calcium malabsorp¬ tion (Schneider et al 1977;Petith & Schedi 1978) and hypercalciuria (Hough et al 1981) in STZ diabetic rats have been demonstrated to be im¬ proved after insulin administration. The present study was designed, accordingly, to investigate whether or not these alterations of mineral and vitamin D metabolism in STZ diabetic rats could be normalized by insulin therapy.…”

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confidence: 99%

Effects of insulin on altered mineral and vitamin D metabolism in streptozotocin-induced diabetes

Ishida¹,

Seino²,

Nishi³

et al. 1985

Acta Endocrinologica

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In order to ascertain whether or not abnormal mineral and vitamin D metabolism in diabetes can be reversed by insulin therapy, plasma calcium, ionized calcium, phosphorus, parathyroid hormone (PTH) and vitamin D metabolites were measured in control, streptozotocin (STZ) diabetic and insulin-treated diabetic rats. Blood glucose levels in diabetic rats treated with insulin decreased to normal. The low plasma calcium and ionized calcium levels in diabetic rats were found to be normal in insulin-treated diabetic rats. An elevated PTH level was observed in the diabetic group, but it was at normal levels in the insulin-treated diabetic group.Plasma 25-hydroxyvitamin D (25(OH)D) and 24,25-dihydroxyvitamin D (24,25(OH)2D) in the diabetic group were decreased compared to those in control rats, but these were also fully restored to control levels by insulin therapy. However, plasma 1,25-dihydroxyvitamin D (1,25(OH)2D) levels in the untreated diabetic group tended to be lower than in controls, and the values in insulin-treated rats were significantly decreased compared to the control group. The ratio of 1,25(OH)2D to 25(OH)D in diabetic rats was higher than in controls, but it was decreased after insulin therapy and was significantly lower than in the control group. It is suggested, therefore, that the negative calcium balance and decreased 25(OH)D and 24,25(OH)2D levels are derived from the metabolic derangement due to the insulin deficiency. Furthermore, insulin seems to suppress the conversion of 25(OH)D to 1,25(OH)2D in experimental diabetes in vivo. Some investigators have reported that mineral and bone metabolism is altered both in human (McNair et al. 1979) and experimental (Hough et al. 1981) diabetes. We have previously studied the serial changes of mineral and vitamin D metabolism in streptozotocin (STZ) diabetic rat and have found that plasma calcium, 25-hydroxyvitamin D (25(OH)D) and 24,25-dihydroxyvitamin D (24,25 (OH)2D) levels are decreased at the later stage of diabetes (Ishida et al. 1983a). McNair et al. (1983) have also demonstrated that serum ionized calcium concentrations are decreased in insulin-dependent diabetic patients. On the other hand, it has been shown that hypercalciuria in diabetic patients is ameliorated with insulin therapy (Raskin et al. 1978). Furthermore, intestinal calcium malabsorp¬ tion (Schneider et al. 1977;Petith & Schedi 1978) and hypercalciuria (Hough et al. 1981) in STZ diabetic rats have been demonstrated to be im¬ proved after insulin administration. The present study was designed, accordingly, to investigate

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“…Ileal calcium transport requires longer duration of diabetes for the defect to become evident, suggesting greater resistance of ileal transport to vitamin D depletion or maintenance of transport by lower concentrations of 1,25-(OH)ZD. The calcium transport response pattern of the ileum to diabetes resembles that of the large intestine: cecal and colonic calcium transport are not decreased until 1 1-14 days of diabetes (9). Thus, in experimental diabetes gut sites show individual time course patterns with respect to depression of calcium transport.…”

mentioning

confidence: 90%

Small Intestinal Calcium Absorption in the Rat with Experimental Diabetes

Walker

Schedl

1979

Experimental Biology and Medicine

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We previously studied downhill calcium absorption in the diabetic rat (luminal concentration 3.4 mM, serum ionized calcium, 1-1.1 mM): Duodenal absorption by diabetics was half that of controls whereas ileal absorption was normal (1). Although vitamin D intake and absorption of fat are normal in diabetic rats (l), we subsequently found vitamin D metabolism to be abnormal: serum concentrations of 1,25-dihydroxyvitamin D (1,25-(OH),D) in diabetics are one-eighth the levels in controls (2). Since 1,25-(OH)2D is the active metabolite of vitamin D that acts directly on the gut, the depression of 1,25-(OH),D concentration explains the decreased duodenal calcium absorption. Unexplained is the lack of effect of diabetes on ileal calcium absorption, since the ileum responds to vitamin D depletion and repletion (3). Since we had studied only downhill calcium absorption and had examined diabetics during the 5-to 10-day time span after injection (l), it was possible that we did not detect an effect of diabetes on ileal transport because of the luminal calcium concentration used or the time span after induction of diabetes selected for study (1). We therefore examined the effects of diabetes on duodenal and ileal calcium transport early (4 days) and late (11 days) after induction of diabetes and at luminal calcium concentraions below and above serum ionized calcium.Materials and Methods. We used male Sprague Dawley derived rats (Simonsen Labs, Gilroy, CA) housed in air-conditioned quarters and fed Teklad diet (1.5% calcium; 1.3% phosphorus). Animals to be made diabetic received intraperitoneal streptozotocin freshly prepared in citrate buffer, pH 4.5. The initial dose was 100 mg/kg body wt and 24 hr later they received a second injection of 25 mg/kg. Controls received similar injections of buffer alone. Diabetes was assessed by loss of body weight, glycosuria and elevated fasting blood glucose. To measure absorption, rats were anesthetized with intraperitoneal Nembutal and perfused in vivo by recirculating 10 ml of solution at a pump rate of 2.0 ml/min for 2 hr. Absorption was studied following an overnight fast at 4 days and I 1 days after injection of streptozotocin. The first 10 cm of duodenum and last 15-20 cm of ileum were perfused in each rat, and control and diabetic rats were always studied at the same time. Perfusates contained 0.8 mM calcium or 3.4 mM calcium, 45Ca (12 &liter, initial specific activity 2000 pCi/mg, New England Nuclear Corp.), 165 mM NaC1, and 50 mg/l phenol red.At the conclusion of perfusion blood was drawn from the inferior vena cava to measure glucose in serum (4). The duodenal and ileal segments were removed, measured for length, weighed, and the mucosa scraped from the underlying tissue. Total wet weight and total length of the small intestine were also obtained. Tissues were dried for 24 hr at 100" in a vacuum oven and reweighed to obtain dry weight. Calcium was measured by atomic absorption spectrometry in test solutions and luminal perfusates. 45Ca was measured by liquid scintillation countin...

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Effects of diabetes on cecal and colonic calcium transport in the rat.

Cited by 10 publications

References 15 publications

Effects of Diabetes on Calcium-Binding Protein in the Cecum and Colon of the Rat

Effects of Diabetes on Calcium-Binding Protein in the Cecum and Colon of the Rat

Effects of insulin on altered mineral and vitamin D metabolism in streptozotocin-induced diabetes

Small Intestinal Calcium Absorption in the Rat with Experimental Diabetes

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