Renal calcium and magnesium handling in experimental diabetes mellitus in the rat

Anwana, A. B.; Garland, Hugh

doi:10.1530/acta.0.1220479

Cited by 26 publications

(49 citation statements)

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“…The results from these studies clearly indicate that diabetic animals have hypercalciuria, decreased circulating 1,25(OH)2D3, and reduced bone mass. While hypercalciuria occurs, plasma levels of ionized and total Ca 2+ can be maintained at normal levels in several study models [7][8][9]34]. These data implicate that a compensatory mechanism for diabetes-induced renal Ca 2+ loss exists.…”

Section: Discussionmentioning

confidence: 98%

“…Hypercalciuria is commonly associated with diabetes [4][5][6][7][8][9]. However, the number of studies addressing the pathophysiology of altered Ca 2+ homeostasis during diabetes [7][8][9]34] is limited. The results from these studies clearly indicate that diabetic animals have hypercalciuria, decreased circulating 1,25(OH)2D3, and reduced bone mass.…”

Section: Discussionmentioning

confidence: 99%

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Proteomic Identification and Immunolocalization of Increased Renal Calbindin-D28k Expression in OVE26 Diabetic Mice

Thongboonkerd¹,

Zheng²,

McLeish³

et al. 2005

Rev Diab Stud

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■ AbstractDiabetic nephropathy is a common diabetic complication that is associated with alterations in the expression of several renal proteins and abnormal calcium homeostasis. We performed proteomic analysis to screen for global changes of renal protein expression in diabetic kidney. Proteins extracted from the whole kidney of 120-day-old OVE26 (a transgenic model of Type 1 diabetes) and FVB (non-diabetic background strain) mice were separated by two-dimensional polyacrylamide gel electrophoresis (2-D PAGE) and visualized by SYPRO Ruby staining (n = 5 in each group). Quantitative intensity analysis revealed 41 differentially expressed proteins, of which 30 were identified by matrix-assisted laser desorption/ionization-time-of-flight mass spectrometry (MALDI-TOF MS) followed by peptide mass fingerprinting. One of the altered proteins with the greatest magnitude of change was the calcium-binding protein, calbindin-D28k, whose expression was increased 6.7-fold in diabetic kidney. We confirmed the increase in calbindin-D28k expression in diabetic kidney by Western blot analysis. Immunohistochemical study demonstrated that calbindin-D28k expression was markedly increased in tubular epithelial cells of distal convoluted tubules (DCT), collecting ducts (CD), and proximal convoluted tubules (PCT) in diabetic kidney. Calbindin-D28k plays a critical role in maintaining calcium homeostasis. The elevation in renal calbindin-D28k expression in our model may indicate a compensatory mechanism to overcome hypercalciuria in diabetes.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Proteomic Identification and Immunolocalization of Increased Renal Calbindin-D28k Expression in OVE26 Diabetic Mice

Thongboonkerd¹,

Zheng²,

McLeish³

et al. 2005

Rev Diab Stud

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“…Low turnover osteopenia with reduced mineral content has also been well documented in experimental models of IDDM, such as streptozotocin-induced (Ishida et al 1988) and spontaneous rat diabetes (Verhaeghe et al 1989(Verhaeghe et al , 1990. Another prominent feature of human and experimental IDDM is an increased urinary excretion of calcium and magnesium (Raskin, Stevenson, Barilla & Pak, 1978;Anwana & Garland, 1990). Plasma calcium concentration in the rat is normally maintained in the face of such renal losses (Anwana & Garland, 1990).…”

Section: Introductionmentioning

confidence: 99%

“…Another prominent feature of human and experimental IDDM is an increased urinary excretion of calcium and magnesium (Raskin, Stevenson, Barilla & Pak, 1978;Anwana & Garland, 1990). Plasma calcium concentration in the rat is normally maintained in the face of such renal losses (Anwana & Garland, 1990). A decreased bone mineral content may therefore represent an I I Corresponding author: hgarland@ fs 1.scg.man.ac.uk unfortunate consequence of the marked hypercalciuria serving to maintain normocalcaemia under these conditions.…”

Section: Introductionmentioning

confidence: 99%

Bone mineral density and composition in rat pregnancy: effects of streptozotocin‐induced diabetes mellitus and insulin replacement

Tein¹,

Breen²,

Loveday³

et al. 1998

Experimental Physiology

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SUMMARYA disturbed calcium homeostasis characterizes diabetic pregnancy. This study documents changes in bone mineral composition in diabetic pregnant rats and examines the effect of insulin replacement. Control pregnant (CP), diabetic pregnant (DP) and insulin-treated DP (DP1) rats were assessed for femoral calcium and magnesium content, bone mineral density (BMD) and the ratio of hypertrophic to maturing and proliferative cells in the femoral growth plate. DP rats showed a significantly (P < 0.01) lower body weight, femoral weight and length than CP rats. Femoral calcium and magnesium content was also significantly (P < 0.05) lower in DP rats, as was ash weight. When calcium and magnesium were normalized for ash weight no signflcant differences were apparent. A significantly (P < 0.05) lower total BMD at the distal femur was seen in DP rats. This comprised a significantly (P < 0.01) lower trabecular BMD with no significant change in cortical BMD. A significantly (P < 0.05) higher ratio of hypertrophic to maturing and proliferative cells of the femoral growth plate was evident in DP animals. DPi rats showed normal blood glucose concentrations and femoral growth plate histology. DPi rats also showed normal femoral weight and length but only partially restored femoral ash weight and mineral content. Insulin failed to normalize total or trabecular BMD. Diabetes mellitus clearly has a marked effect on bone growth and mineral content in pregnancy which may be relevant to overall calcium homeostasis. The lower bone growth, bone calcium content and trabecular BMD may be unfortunate consequences of the marked hypercalciuria reported elsewhere in diabetes and may serve to maintain normocalcaemia in the disease.

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“…[1][2][3] The low levels are attributed to glucosuriarelated increased renal magnesium loss. 2,4 Hypomagnesaemia has been associated with decreased glucose disposal both in patients with Type 2 DM and in non-diabetic subjects. 5 Paolisso et al have shown that oral magnesium supplementation in patients with Type 2 DM and mildly decreased plasma magnesium levels improves insulin sensitivity and secretion.…”

Section: Introductionmentioning

confidence: 99%

Oral magnesium supplementation in insulin-requiring Type 2 diabetic patients

Valk

Verkaaik²,

Rijn³

et al. 1998

Diabet. Med.

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Oral magnesium (Mg) supplementation can improve insulin sensitivity and secretion in patients with Type 2 diabetes mellitus (DM). We studied the effect of Mg supplementation on glycaemic control, blood pressure, and plasma lipids in insulin-requiring patients with Type 2 DM. Fifty moderately controlled patients were randomized to 15 mmol Mg or placebo daily for 3 months. Plasma Mg, glucose, HbA1c, lipids, erythrocyte Mg, Mg and glucose concentrations in 24-h urine, and systolic and diastolic pressure were measured before and after 3 months treatment. Plasma Mg concentration was higher after supplementation than after placebo (0.82 +/- 0.07 vs 0.78 +/- 0.08 mmol l(-1), p < 0.05), as was Mg excretion (5.5 +/- 1.9 vs 3.7 +/- 1.4 mmol 24 h(-1), p = 0.004) but erythrocyte Mg concentrations were similar. No significant differences were found in glycaemic control (glucose: 10.7 +/- 3.8 vs 11.6 +/- 6.2 mmol l(-1), p = 0.8; HbA1c: 8.9 +/- 1.6 vs 9.1 +/- 1.2%, p = 0.8), lipids or blood pressure. On-treatment analysis (34 patients: 18 on Mg, 16 on placebo) yielded similar results. An increase in plasma Mg concentration irrespective of medication was associated with a tendency to a decrease in diastolic pressure (increased plasma Mg vs no increase: -4.0 +/- 10.1 vs +2.5 +/- 12.0 mmHg, p = 0.059). Three months' oral Mg supplementation of insulin-requiring patients with Type 2 DM increased plasma Mg concentration and urinary Mg excretion but had no effect on glycaemic control or plasma lipid concentrations.

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Renal calcium and magnesium handling in experimental diabetes mellitus in the rat

Cited by 26 publications

References 0 publications

Proteomic Identification and Immunolocalization of Increased Renal Calbindin-D28k Expression in OVE26 Diabetic Mice

Proteomic Identification and Immunolocalization of Increased Renal Calbindin-D28k Expression in OVE26 Diabetic Mice

Bone mineral density and composition in rat pregnancy: effects of streptozotocin‐induced diabetes mellitus and insulin replacement

Oral magnesium supplementation in insulin-requiring Type 2 diabetic patients

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