Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 2484 newly detected metabolic bone diseases during the past 17 years comprised 79.67% cases of osteoporoses and 20.33% of osteomalacia. The group of osteoporoses included 325 patients (16.43%) with the primary form of the disease, in 1654 patients (83.57%) a cause of decalcification of bones (secondary form) was found. With advancing time the number of secondary osteoporoses rises steadily, while the number of primary cases remains at the same level. In the aetiology of demineralization a major part was played by lactose intolerance, maldigestion and malabsorption, idiopathic, hypercalciuria, diabetes and steroids. The female: male ratio in primary osteoporoses was 4.71:1 and in secondary osteoporoses 2.35:1. Primary osteomalacia was recorded in 113 patients (22.38%) and secondary in 392 (77.62%). Here too with advancing time the number of secondary forms is increasing. The largest groups are hepatic and renal affections, smaller ones malabsorption and antiepileptic drugs. The female: male ratio in primary osteomalacia is 2.13:1 and in secondary osteomalacia 2.26:1. With the development of knowledge on the aetiopathogenesis of bone demineralizations we expect in future a further increase of secondary forms of the disease at the expanse of primary ones.
 ...
PMID:[Secondary osteopenia]. 228 20

The study was aimed at the evaluation of changes in the urinary excretion of calcium in patients with diabetes of type I and II. The investigations were carried out in 34 patients with type I diabetes, 28 patients with type II diabetes and 30 control subjects having the normal glucose tolerance. The oral calcium tolerance test according to Pak was performed in all the patients and the controls. Besides normocalciuria, also hypercalciuria of renal origin, as well as hipercalciuria resulting from an elevated intestinal absorption of calcium have been found in diabetic patients. These disturbances occurred much more frequently in patients with type I diabetes, especially in those of age below 40.
 ...
PMID:[Hypercalciuria in patients with diabetes mellitus type 1 and 2--studies of its pathogenesis using the oral calcium tolerance test]. 262 18

Metabolic studies were performed in streptozotocin-induced diabetic (D) rats and normal control (C) rats to assess the role of hyperphagia in the hypercalciuria of diabetes. Urinary calcium excretion (UCaV) was significantly higher in D v C rats fed ad libitum. When D rats were pair-fed (calorie and mineral restriction) with C rats, UCaV declined but remained significantly higher than in C rats. When D rats were allowed their usual increased calorie intake but restricted to C rat mineral consumption, UCaV remained elevated. These findings suggested a tubular reabsorptive defect. In vivo microinjection studies were then performed to identify the site(s) of the tubular reabsorptive defect. Using 1.0 mmol/L Ca in the injectate, 45Ca recovery in the urine (CaR%) was significantly higher in D rats after intratubular injections into early and late proximal tubules and late distal but not early distal tubules. An additional load-dependent defect was revealed in the terminal nephron when the Ca concentration of the injectate was increased to 1.8 mmol/L. After early distal injection, CaR% was significantly increased in D v C rats. Infusion of PTH into thyroparathyroidectomized C and D rats enhanced Ca absorption to a similar degree but did not correct the reabsorptive defect in D rats. These results argue against a lack of end-organ responsiveness to PTH in diabetes or a low serum PTH level as the cause of the hypercalciuria. We conclude that hyperphagia contributes to the hypercalciuria of diabetes in the absence of increased Ca intake. Also, two tubular reabsorptive defects exist: one in the loop of Henle; the other, load-dependent in the terminal nephron.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The mechanism of hypercalciuria in streptozotocin-induced diabetic rats. 335 15

The role of hypercalciuria and hyperphosphaturia in the growth retardation of children with diabetes mellitus was investigated in 157 children with diabetes whose mean height was less than that of 37 nondiabetic siblings of similar age (P less than .025). Hyperglycemia, hypercalciuria, and hyperphosphaturia were assessed coincident with the height measurement of each child in a cross-sectional survey. The distribution of height percentiles of the children with diabetes was skewed to the left with 61% at or below the 50th percentile. Eleven percent of the insulin-dependent children with diabetes mellitus were shorter than would be anticipated by a normal distribution of the 157 children. The duration of diabetes (hyperglycemia) had the greatest influence upon the children's height. Children with diabetes were shorter than the nondiabetic subjects by the fourth year of hyperglycemia, and this difference in height became statistically significant after 7 years or more of diabetes. The degree of hypercalciuria and hyperphosphaturia was more closely associated with reduced height in children with diabetes than was the degree of hyperglycemia, although the renal wastage of calcium and phosphorus seemed to be the result of glucosuria. Because hypercalciuria and hyperphosphaturia impair growth in nondiabetic children, they may also play an important role in the poor growth of children with diabetes mellitus.
 ...
PMID:Hypercalciuria, hyperphosphaturia, and growth retardation in children with diabetes mellitus. 348 37

Hematuria of unknown origin occurs in 30% of patients with diabetic nephropathy. In nondiabetic persons, hematuria may be caused by hypercalciuria with or without nephrolithiasis. Eight children with type I diabetes mellitus, hematuria, and hypercalciuria were observed in our clinic during a 1-year period. Two of these also had evidence of renal papillary necrosis. To assess the importance of hypercalciuria in the pathogenesis of hematuria in children with diabetes mellitus, we measured urinary calcium excretion in a large population of such patients. The calcium to creatinine ratio in the urine of diabetic children (0.21 +/- 0.01) was greater than that of nondiabetic children (0.12 +/- 0.01). A calcium to creatinine ratio of 0.28 was established as the upper limit of normal in our nondiabetic population, and 27% of the diabetic children were hypercalciuric on this basis. The diabetic children with hypercalciuria also had hyperphosphaturia and a urinary CaHPO4 X 2H2O molar ion product three times that found in the nondiabetic control population. These data suggest that many children with diabetes are at risk for renal damage due to hypercalciuria. Because hypercalciuria is more common in diabetic than nondiabetic children, it may play a previously unrecognized role in the renal disease associated with diabetes mellitus.
 ...
PMID:Hematuria and hypercalciuria in children with diabetes mellitus. 357 34

This study reports a 22% prevalence of significant cortical osteopenia in 206 patients, aged 7-20 years, with established insulin-dependent diabetes mellitus (IDDM). A parallel decrease in trabecular bone mass was also noted. Bone loss was more evident in males (16%) than in females (6%) and was rare before 10 years of age (3%). No relationship between bone loss and the duration of diabetes, degree of metabolic control or diabetic complications was apparent. Delayed skeletal maturation did not account for cortical thinning, and the mean bone age of osteopenic diabetics was similar to that of non-osteopenic diabetics. There was no significant correlation between HLA-antigen frequency and the predisposition to diabetic osteopenia. Metabolic alterations comparable with previous findings in the chronically diabetic rat were documented in IDDM. The data documented are consistent with the conclusion that IDDM results in intestinal hyperabsorption of calcium, absorptive hypercalciuria, phosphaturia, hypomagnesaemia, hyperphosphatasaemia, and decreased circulating parathyroid hormone levels. These alterations in mineral metabolism may relate to the decrease in cortical and trabecular bone mass observed in patients with IDDM.
 ...
PMID:Alterations of bone and mineral metabolism in diabetes mellitus. Part II. Clinical studies in 206 patients with type I diabetes mellitus. 361 83

Calcium and vitamin D metabolism were studied in streptozotocin-treated rats up to 10 days after the induction of diabetes. Proteinuria, hypercalciuria, and hyperphosphaturia appeared as early as 3 days after diabetes induction and were reversed by insulin. The serum proteins and fasting calcium concentrations were decreased in untreated diabetic rats. The concentration of serum vitamin D binding protein (DBP) was higher in male than in female control rats (mean +/- SD; 555 +/- 73 vs. 348 +/- 28 mg/liter, P less than 0.001). When sequentially measured in male untreated diabetic rats, DBP concentration steadily decreased. Compared with control values, DBP was reduced 19%, 28%, and 32% on days 3, 6, and 10, respectively, after induction of diabetes in male rats. In female animals, DBP was reduced 22% on day 10 of diabetes. DBP concentration was corrected by insulin treatment of diabetic rats and remained normal in streptozotocin-treated animals that did not develop diabetes. The serum concentration of 25-hydroxyvitamin D3 was similar in both sexes and was not affected by diabetes. Like DBP, the concentration of total 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] was higher in male than in female control rats (120 +/- 24 vs. 96 +/- 17 ng/liter, P less than 0.001), but 10 days after induction of diabetes this concentration decreased by 37% and 29% in male and female rats, respectively. The free 1,25-(OH)2D3 concentration, estimated from the molar 1,25-(OH)2D3/DBP ratio, was similar in both sexes and was not decreased by diabetes. We conclude that experimental diabetes in the rat induces a decrease in DBP concentration and a concomitant decrease in total but not in free 1,25-(OH)2D3 concentrations. This may indicate that diabetes decreases circulating 1,25-(OH)2D3 concentrations through alterations in DBP levels.
 ...
PMID:1,25-Dihydroxyvitamin D and vitamin D-binding protein are both decreased in streptozotocin-diabetic rats. 383 33

Calcium homeostasis was studied in freely fed control, streptozotocin diabetic, long-term and short-term insulin-treated diabetic rats 7 wk after the induction of diabetes. In contrast to the short-term (5-12 day) diabetic rat model, intestinal absorption of calcium was markedly enhanced in chronically insulin-deficient animals. Moreover, conventional balance studies showed that these animals were in positive calcium balance despite severe hypercalciuria. Intestinal hyperabsorption of calcium in long-standing diabetic rats occurred despite low levels of circulating 1,25-dihydroxyvitamin D and hypercorticosteronism and was attended by hypercalcemia and suppression of both plasma parathyroid hormone (PTH) and urinary cyclic 3',5'-AMP (cAMP). Long-term insulin replacement completely normalized the intestinal hyperabsorption of calcium, corrected the plasma calcium, and significantly increased circulating PTH and urinary cAMP excretion. Insulin therapy also corrected the decreased plasma 1,25-dihydroxyvitamin D observed in untreated diabetic animals. Intestinal hyperabsorption of calcium appeared to be only partially corrected by short-term insulin therapy. The accumulated results reveal decided differences in calcium homeostasis and hormonal response between the rats with long-standing diabetes and those with diabetes of short duration.
 ...
PMID:Calcium homeostasis in chronic streptozotocin-induced diabetes mellitus in the rat. 628 97

Diabetes mellitus was induced in Lewis rats by streptozotocin, and these animals and control rats fed ad lib were studied after 7 weeks. At the time of sacrifice, nondecalcified histological sections of bone were prepared and subsequently quantitated by micromorphometric techniques. In addition, tibial alkaline phosphatase and mineral ash content were determined. The bones obtained from the diabetic animals are characterized by significant decrements in the quantities of osteoid and osteoclasts and by failure to acquire a tetracycline label. These histological features are attended by reduced quantities of urinary hydroxyproline and tibial alkaline phosphatase. As compared with control animals fed ad lib, diabetic rats are hyperphosphatemic and markedly hypercalciuric. Circulating alkaline phosphatase is also elevated and associated with a parallel increase in intestinal content of this enzyme. Although serum corticosterone levels are increased, diabetes is associated with decrements in both circulating immunoreactive parathyroid hormone and 1,25(OH)2D. We conclude that prolonged streptozotocin-induced diabetes mellitus in the rat results in reduced bone turnover. The relative roles that functional caloric deprivation, low circulating levels of 1,25(OH)2D, hypercalciuria, hypercortisolemia, and decreased blood parathyroid hormone levels play in the genesis of these skeletal abnormalities remain to be determined.
 ...
PMID:The effect of streptozotocin-induced chronic diabetes mellitus on bone and mineral homeostasis in the rat. 645 Feb 54

Of 117 formers of relapsing calcium oxalate calculi 75.2% showed a hyperuricaemia, 64.1% a hyperlipoproteinaemia, 19.7% a diabetes mellitus, 44.4% a hypertension, 11% a hyperuricuria (greater than 1.0 g/a day) and 7.5% a hypercalciuria. In 30 formers of relapsing uric acid calculi we could establish a hyperuricaemia in 93.3%, a hyperlipoproteinaemia in 76.7%, a diabetes mellitus in 36.7%, a hypertension in 80%, a hyperuricuria in 11% and a hypercalciuria in 3.8%. In comparison to formers of calcium oxalate calculi patients with uric acid calculi had a significantly higher body-weight. The results of our examinations make clear that in relapsing formation of urinary calculi frequently a complex disturbance of the metabolism is present which in every case must be established and treated.
 ...
PMID:[Incidence of metabolic disorders in patients with recurrent urinary calculi]. 722 5


<< Previous 1 2 3 4 5 6 7 Next >>