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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dietary boron, in concentrations similar to that found in human diets comprised mainly of fruits and vegetables, affects both mineral and energy metabolism. Therefore, the effects of boron on a model system with a perturbed metabolic insulin-vitamin D3 axis was examined. Weanling male rats were fed a ground corn-high protein casein-corn oil-based diet (0.06 mg B/kg; no supplemental vitamin D3) supplemented with B (as orthoboric acid) at 0 or 2.4 mg/kg. After 55 days, all rats were equilibrated in individual metabolic cages for 6 days. After another 6 days, one half of the rats in both dietary groups were injected intraperitoneally with streptozotocin (STZ). All rats were killed 3 days after STZ treatment. STZ affected many aspects of mineral metabolism as expected. Plasma ionized calcium concentrations fell by approximately 10% in STZ-treated rats. Brain and heart mineral metabolism was spared from the toxic effects of STZ whereas spleen mineral metabolism was especially vulnerable to STZ. Supplemental dietary boron increased urinary excretion of calcium in the non-STZ rats but did not affect the plasma concentrations of alkaline phosphatase, ionized calcium or the concentration of calcium in the brains, lungs, kidneys and spleens of those animals. Supplemental dietary boron temporarily reduced the abnormally elevated renal excretion of albumin, potassium and sodium during the acute phase of diabetes mellitus. On the other hand, physiological amounts of dietary boron exacerbated the abnormally elevated rate of collagen breakdown in the STZ animal. Finally, boron may have indirectly affected heart mineral metabolism because dietary boron did not affect cardiac boron concentrations but did affect cardiac copper, calcium, manganese, molybdenum and phosphorus concentrations, primarily in non-STZ rats. The findings suggest that dietary boron has both protective and regulatory roles in mineral metabolism.
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PMID:Effects of dietary boron on calcium and mineral metabolism in the streptozotocin-injected, vitamin D3-deprived rat. 166 22

Sorbitol-3-phosphate (S3P) and fructose-3-phosphate (F3P) are novel phosphorus compounds recently discovered and identified in the crystalline lens as well as other tissues. These phosphates increased with diabetes progression in streptozotocin-diabetic rat lenses. Treatment of these rats with an orally administered aldose reductase inhibitor eliminated S3P and intramuscularly injected insulin obliterated F3P. These results indicate that enzymes catalyzing S3P and F3P formation co-activate with aldose reductase activation and hyperglycemia, respectively.
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PMID:The effect of insulin and aldose reductase inhibition on the phosphate metabolism of streptozotocin-diabetic rat lens. 178 17

To investigate the parathyroid function in diabetes mellitus, we performed an oral phosphate load in 6 diabetic patients and 6 nondiabetic subjects without renal failure (serum creatinine less than 1.5 mg/dl). Each subject received a total of 2.0 g of phosphate daily per os on 5 consecutive days. Blood and urine samples were obtained daily before and 2 h after the administration of phosphate in the morning. All subjects responded with a similar increase in the serum phosphorus concentration and fall in the ionized calcium concentration. Intact parathyroid hormone levels rose by 2.6-fold in the control subjects but by less than 1.5-fold in the diabetic subjects. It was concluded that hyporesponsiveness of the parathyroid hormone to phosphate administration was found in the diabetic patients without renal failure.
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PMID:Parathyroid hormone secretion in diabetes mellitus. 195 50

A retrospective study was done in 86 patients on dialysis in order to evaluate the doses of aluminum hydroxide (OH3 Al) received to achieve a better serum phosphate control. Thirty-seven patients were treated with continuous ambulatory peritoneal dialysis (CAPD) divided in 22 diabetics and 15 non-diabetics. Forty-nine patients were treated with hemodialysis (HD), 12 diabetics and 37 non-diabetics. The doses of 1-25 Dihidroxycholecalciferol (1-25 DOH-D3) were similar in all patients. The serum phosphate levels were similar in CAPD and HD patients with smaller doses of OH3 AL in CAPD patients (p less than 0.001). Diabetics on either technique need less OH3 AL in CAPD (CAPD p less than 0.01; HD p less than 0.05) to achieve the same or better control of serum phosphorus than non-diabetics. The overload of glucose on CAPD and the maintained hyperglycemia on diabetes mellitus would shift phosphorus into the cell and could explain these results. Finally, the less needs of aluminum hydroxide on diabetic patients could contribute to their protection against aluminum deposition and its effects.
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PMID:Diabetic patients on CAPD need less aluminum hydroxide as a phosphate binder than non-diabetics. 198 39

In diabetic animals, there is a decrease in serum 1,25-dihydroxyvitamin D [1,25(OH)2D] and in renal production of 1,25(OH)2D. In nondiabetic animals, renal 1,25(OH)2D production is markedly stimulated by parathyroid hormone (PTH) and calcitonin (CT). There is evidence that diabetes impairs the responsiveness of the kidney to PTH. The effect of diabetes on responsiveness to CT is unknown. The studies reported here determined the effect of streptozotocin-induced diabetes on renal responsiveness to PTH and CT. Experiments were performed in 7- to 8-week-old rats that were fed a diet sufficient in calcium and vitamin D and were thyroparathyroidectomized (TPTX) 5 days before hormone treatment. PTH (0.33 U/g body weight at 24, 12, and 2 hours before death) significantly increased renal 1,25(OH)2D production by threefold in nondiabetic rats. This effect was markedly attenuated by diabetes. On the other hand, CT (20 U/100 g body weight at 12 and 2 hours before death) produced a maximal response in both groups of animals. In diabetic rats, CT stimulated renal 1,25(OH)2D production fivefold, whereas PTH stimulated production only 1.5-fold. Diabetes did not affect the capacity of PTH to increase serum calcium or decrease renal tubular reabsorption of phosphorus (TRP). These findings suggest that the decrease in renal 1,25(OH)2D production seen in experimental diabetes may be due to decreased renal responsiveness to PTH, but not to decreased responsiveness to CT.
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PMID:Calcitonin stimulates 1,25-dihydroxyvitamin D production in diabetic rat kidney. 198 64

We describe the clinical outcome of 13 patients with non-insulin-dependent diabetes mellitus (NIDDM), renal insufficiency, and proteinuria, treated for 12.2 +/- 12.9 months (mean +/- SD) with a low-protein, very-low-phosphorus diet (LPVLP) containing 30 g protein and 11.3 mmol (350 mg) phosphorus. After a control period of 18.2 +/- 20.4 months, LPVLP therapy was initiated and serum urea nitrogen, uric acid, and phosphate, as well as urinary excretion of protein, creatinine, urea nitrogen, uric acid, and phosphate, decreased significantly. There was no change in mean blood pressure, hemoglobin, blood pH, and HCO3-, as well as in serum creatinine, protein, albumin, calcium, magnesium, cholesterol, triglyceride, beta-lipoprotein, and high-density lipoprotein (HDL)-cholesterol. Nitrogen balances were measured over 5 weeks in nine patients. Nitrogen balance increased significantly from a negative balance of -0.795 +/- 1.367 g/d in the first week, to almost neutral in the fourth week, and later, was neutral or positive. Neither uremic symptoms nor signs of malnutrition appeared during the LPVLP period. These results suggest that negative nitrogen balance during the initial few weeks does not predict future nutritional status of patients with diabetic renal failure.
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PMID:Effect of low-protein, very-low-phosphorus diet on diabetic renal insufficiency with proteinuria. 206 52

Alloxan-diabetic rats and age-matched controls were killed after 6 weeks of diabetes; heart and kidneys were removed and assayed for thiobarbituric acid-reactive substances (TBARS), lipid hydroperoxides, lipid phosphorus, total fatty acid composition and glutathione. Tissue homogenates from a second group of diabetic and control rats were incubated in oxygen-saturated buffer with and without the free radical generating system Fe2+/ascorbate (0.1/1.0 mM) and were assayed for lipid peroxidation. Diabetic hearts contained markedly lower levels of TBARS and lipid hydroperoxides (40% and 18%, respectively) than control hearts, whereas differences in TBARS were less pronounced in kidneys (9%). Incubation of homogenates of both organs in the presence or absence of Fe2+/ascorbate for up to 2 h yielded significantly lower levels of TBARS and lipid hydroperoxides with diabetic tissue. Diabetic hearts and kidneys contained higher levels of glutathione (28% and 13% over controls) and both diabetic tissues showed much higher linoleate/arachidonate ratios than did the controls (9.86 vs. 2.56 for heart, 2.01 vs. 0.86 for kidney). We conclude that diabetic tissues develop enhanced defense systems against oxidative stress and we assume tha the lower levels of arachidonate contribute to their resistance to lipid peroxidation as well.
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PMID:Diabetic heart and kidney exhibit increased resistance to lipid peroxidation. 212 2

The basic prerequisite of treatment of diabetic osteopenias is perfect metabolic compensation of diabetes. Insulin administration is an advantage in this respect, as it enhances calcium absorption from the gut and reduces its urinary excretion. Conversely, oral antidiabetics interfere in a negative way with vitamin D metabolism and thus also calcium metabolism and mineralization of bone. The combination of calcium, small doses of vitamin D, NaF and exercise used in the treatment of diabetic osteoporoses leads in general to a significant rise of the calcium serum level, an insignificant rise of the phosphorus level and it reduces alkaline phosphatase activity. A certain disadvantage is the elevated urinary calcium excretion. The main drug in diabetic osteomalacia are usually large doses of vitamin D. The rise of the serum calcium level improves the metabolic compensation of diabetes in a linear fashion. Thiazide diuretics used to reduce excessive calciuria cause slight deterioration of the glucose tolerance but the compensation does not cause major difficulties.
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PMID:[Diabetic osteopathies. 6. Treatment and its pitfalls]. 213 68

Urinary excretion of calcium, inorganic phosphorus, magnesium, glucose, and creatinine was measured in first-void spot urine samples collected 4 days apart in 220 insulin-dependent diabetic (IDDM) children (mean age 11.9 yr) attending a summer camp. A single control urine sample was obtained from 33 healthy nondiabetic siblings (mean age 11.2 yr). Mean +/- SD urinary calcium-creatinine ratios (UCa/Cr) did not significantly differ between IDDM and control subjects (0.14 +/- 0.09 vs. 0.12 +/- 0.09, respectively, P = 0.156). Mean urinary magnesium-creatinine ratios (UMg/Cr) were elevated in IDDM compared with control subjects (0.15 +/- 0.06 vs. 0.08 +/- 0.03, respectively, P = 0.0001). Similarly, mean urinary phosphorus-creatinine ratios (UP/Cr) were significantly increased over those in control subjects (1.12 +/- 0.33 vs. 0.40 +/- 0.22, respectively, P = 0.0001). UCa/Cr, UMg/Cr, and UP/Cr were correlated with increasing mean urine glucose content (P = 0.0001). No correlations were found when UCa/Cr, UMg/Cr, or UP/Cr were compared with patient age, duration of diabetes, glycosylated hemoglobin, or insulin dosage. Urine losses of phosphorus and magnesium were present even when glycemic control was considered good by several methods (glycosylated hemoglobin, short-term glycemic index, or urinary glucose content). Glomerular hyperfiltration was unable to account for increased urinary mineral content. In conclusion, the data indicate that urinary excretion of phosphorus and magnesium is elevated in children with IDDM, regardless of glycemic control. In the presence of glucosuria, this loss is further enhanced. Urinary calcium excretion is significantly higher only during periods of glucosuria. The data suggest that children with IDDM could be at risk for mineral deficiencies in the absence of intensive insulin management.
Diabetes Care 1990 Apr
PMID:Hyperphosphaturia and hypermagnesuria in children with IDDM. 218 Jun 62

Experimental diabetic and galactosemic animal models are widely used to study diabetes-induced complications. Galactose feeding can rapidly produce cataract, retinopathy and nephropathy; it is therefore favored over the diabetic model. Although the common feature for both models is the activation of aldose reductase, there are substantial differences between the two--not only does the rate of cataract progression differ but the metabolic patterns are far more complex than for polyol production alone. We here present the result of a comparison between diabetic and galactosemic lenses and show the differences in phosphorus and aldose metabolism, cell integrity and osmotic environment.
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PMID:Metabolic studies of galactosemic cataract. 220 47


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