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

The authors investigated in a group of 38 subjects with type I diabetes and 222 subjects with type II diabetes laboratory values indicating the level of bone metabolism: calcium, phosphorus, alkaline phosphatase activity in serum, urinary calcium excretion, and they compared the values mutually and with the level of bone mineralization. The authors found significantly lower serum calcium values in all investigated groups, the lowest ones in women with type II diabetes. To these values corresponded always reduced values of bone mineralization which were also lowest in women with type II diabetes. The very lowest bone mineralization was found in groups of subjects treated with oral antidiabetics, the values in women being lower than in men. The authors found also a higher alkaline serum phosphatase activity, in particular of its bone isoenzyme. The significant correlation between the reduced serum calcium value and bone mineralization indicates that this laboratory value has a decisive influence and importance in the development of osteoporosis. The high alkaline phosphatase activity suggests that there is also prescut osteomalacia.
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PMID:[Diabetic osteopathy. 4. Laboratory findings]. 237 77

Adult male and female rats were used as test animals. The experimental diabetes mellitus was provoked with one dose of i.v. injection of streptozotocin (65 mg/kg body weight), which interferes with the insulin release mechanism in pancreatic beta cells. After a follow-up period of 10 wk an average loss of 10% of body weight and an increase of 25% in the amount of blood obtained by decapitation was recorded in the test animals. The biochemical assays performed on the serum of the diabetic rats showed, for both sexes, a fourfold rise in the plasma glucose level, a threefold rise in plasma alkaline phosphatase activity and plasma alanine transferase activity as well as a 1.5-fold rise in plasma creatine value. The two latter values indicated systematic disorders reflected in the liver and the kidneys. An increase in serum total calcium and hydroxyproline values was also detected. The clinical studies of the gingiva showed diminished tissue resistance in diabetic rats. The histologic studies of alveolar bone revealed retarded formation of bone matrix and new bone in diabetic animals. However, the stimulated metabolism in alveolar bone, due to the artificially induced stress, increased marginal bone cell activity in both the diabetic and the control group, resulting in increased crestal resorption in the former group. The differences in tissue response observed among the diabetic animals affected and unaffected by stress originated from the disturbed recovering mechanism typically found in diabetic animals.
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PMID:Impact of streptozotocin-induced diabetes on rat blood and alveolar bone affected by occlusal stress. 252 6

Data on the function of neutrophils in diabetes mellitus not infrequently accompanied by inflammatory complications are scarce. The aim of this work is to investigate the state of some components of neutrophil granules (cationic proteins, activity of myeloperoxidase, alkaline phosphatase) that play a major role in the mechanisms of destruction of microorganisms in phagocytosis.
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PMID:[The activity of cationic proteins, peroxidase and alkaline phosphatase in the blood neutrophils of diabetics]. 255 45

The urinary excretion of kidney-specific marker proteins before and 120 hours after intravenous injection of either high- or low-osmolar contrast media (CM; diatrizoate, iopamidol 370) was monitored in patients after digital vascular imaging. Inclusion criteria for the randomized clinical study in a total of 40 patients (15 women, 25 men; mean age, 64.5 years) were at least 50 years of age or diabetes mellitus with normal creatinine concentration in serum. Compared with the control period, the elimination of tubular indicator enzymes alanine aminopeptidase, gamma-glutamyltranspeptidase, alkaline phosphatase, as well as of glomerular localized angiotensinase A was significantly higher in all patients after injection of the CM. The most significant differences were observed after 48 hours. In contrast, lysosomal N-acetyl-beta-D-glucosaminidase activity in urine specimens reacted less clearly and appears to be a less sensitive parameter in assessing CM nephrotoxicity. Elimination of brush border as well as of glomerular marker proteins was significantly lower after intravenous injection of low-osmolar CM iopamidol 370 (832 mOsm/kg) than after meglumine diatrizoate 76 (2100 mOsm/kg). In all 40 patients a significant decrease in creatinine clearance was observed; however, patients receiving diatrizoate had a significant decrease in creatinine clearance (period 0 versus 24 to 48 hours after CM), whereas patients after administration of iopamidol had not. No difference was found between creatinine clearance after 48 hours of CM injection within both groups of CM. Due to noninvasive parameters of kidney damage nonionic, low-osmolar CM are less nephrotoxic in potential risk patients, and should be preferred to conventional CM.
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PMID:Nephrotoxicity of high and low osmolar contrast media: case control studies following digital subtraction angiography in potential risk patients. 256 16

Cytochemical indices of leukocytes were determined in 16 patients with diabetes mellitus in the period of unbalancing and balancing. The following tests were made: content of glycogen and lipids, acid phosphatase (AP), alkaline phosphatase (AIP), myeloperoxidase (MPO) and nonspecific alpha-naphtol acetate esterase (NANAE) activity. In unbalanced diabetics an evident decrease in the activity of AP and MPO could be noted as well as a decrease of glycogen content and an increase of lipid content. An insignificant decrease could be observed in the activity of ALP and NANAE in granulocytes. A slight increase in the activity of NANAE in monocytes would be found. Balancing this disease induced the increase of all parameters in granulocytes except MPO activity. It is interesting to note that balancing diabetes mellitus deepened the observed changes in the decrease or increase of tested parameters. The presented findings clearly indicate the role of metabolic disorders in diabetes mellitus on the activity of some neutrophilic enzymes and the glycogen and the content of lipids in neutrophils.
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PMID:Cytochemical indices of leukocytes in patients with diabetes mellitus. 258 66

To identify early markers of the preclinical stage of diabetic nephropathy, a study was made of the activity of the specific canalicular enzymes in urine: N-acetyl-beta-D-glucosaminidase (NAG), beta-glucuronidase (beta-G1), gamma-glutamyl transferase (GGT), alkaline phosphatase (AP) and lactate dehydrogenase (LDH) in patients with diabetes mellitus without (26) and with (15) proteinuria. Patients without the clinical signs of diabetic nephropathy manifested a significant rise of excretion of lysosomal enzymes of the proximal canaliculi (NAG and beta-G1). Concomitant elevation of the excretion of several enzymes (NAG, beta-Gl, GGT and AP) was observed in 50% of cases. Patients with diabetic nephropathy demonstrated an increase of the excretion of all enzymes under study. Puncture biopsy of the kidneys was made in 4 patients without proteinuria with insignificant duration of diabetes mellitus and concomitant elevation of the excretion of a number of enzymes. Light microscopy revealed minimal changes in the glomeruli, whereas electron microscopy changes both in the glomeruli and in the canaliculi. The morphological changes in renal tissue confirm the diagnostic importance of high concomitant excretion of canalicular enzymes (NAG, beta-Gl, AP) as a marker of the preclinical stage of diabetic nephropathy.
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PMID:[Urinary enzymes as a marker of the preclinical stage of diabetic nephropathy]. 262 51

The changes in blood serum concentrations of calcium, magnesium, inorganic phosphate, total activity of alkaline phosphatase and the activity of its bone fraction, as well as urinary excretion of calcium, phosphate, hydroxyproline and oxalate have been measured in 31 patients with insulin-dependent (type I) diabetes, in 31 patients with non-insulin-dependent (type II) diabetes and in 29 healthy subjects in the condition of low-calcium diet. The elevated urinary excretion of calcium, phosphate, hydroxyproline and oxalate, lowered blood serum level of magnesium, and increased total and bone fraction activities of alkaline phosphatase were found in diabetic patients. The urinary excretion of calcium and hydroxyproline, and the activity of bone fraction alkaline phosphatase were significantly higher in patients with type II diabetes than in those with type I diabetes. It was concluded that there is a significant relation between the state of metabolic normalization of diabetes and the degree of biochemical aberrations concerning calcium-phosphate metabolism.
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PMID:[Selected indicators of calcium-phosphate metabolism in patients with diabetes mellitus]. 264 14

The inhibition of alkaline phosphatase by insulin is a finding reported by many researchers but the mechanism of this inhibition has not been studied. Since alkaline phosphatase is an important factor in the mechanism of calcification and an impairment of mineralisation has been observed in diabetes mellitus, a study was carried out to assess the effect of the hormone on alkaline phosphatase measured in chondrocytes, in matrix vesicles and in a purified enzyme preparation. Enzyme activity was inhibited by insulin. The lowest active concentration was 10(-6) M and maximal inhibition was obtained at about 10(-4) M. The inhibition is of the uncompetitive type. Full recovery of the hormone-inhibited enzyme was obtained with 10(-4) M 2-mercaptoethanol. Data suggest direct interaction between the alkaline phosphatase and insulin molecules, involving either disulfide cross linkages or the metal chelating activity of insulin.
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PMID:Possible mechanism of inhibition of cartilage alkaline phosphatase by insulin. 269 41

A randomized, double-blind, 1-year pilot study of prednisolone treatment for primary biliary cirrhosis was undertaken. Nineteen patients received 30 mg prednisolone per day initially, with a maintenance dose of 10 mg per day. Seventeen patients received placebo. The groups were matched for age, menopausal status, hepatic histological stage and bilirubin. Treatment was well tolerated without dropouts. Two patients receiving prednisolone developed diabetes, one a duodenal ulcer and one depression. One patient receiving placebo died for liver failure after 3 months. Cholestatic symptoms (itch and fatigue) improved on prednisolone. There was significant (prednisolone vs. placebo) improvement in transaminase (p = 0.0214), alkaline phosphatase (p = 0.0032), procollagen III peptide (p = 0.0103), immunoglobulin G (p = 0.0012) and liver histology (p = 0.016); these changes were greatest among noncirrhotic patients. No patient developed skeletal symptoms. Fifty-seven per cent had abnormal triolein breath tests prior to treatment, and 65% had abnormally low calcium absorption tests. Calcium absorption increased significantly in the treated group vs. placebo at 2 weeks (p less than 0.02), but not at 1 year. Femoral photon absorptiometry fell in the prednisolone group after 1 year (-3.5% vs. placebo +0.5%, p less than 0.05), as did trabecular bone volume (-6% vs. -2.8%, p less than 0.005) and resorption surface (-11% vs. +2%, p less than 0.02) on serial bone biopsy. Prednisolone seems to exert a favorable hepatic effect in primary biliary cirrhosis but at the expense of increased bone loss to approximately twice the expected rate. Prednisolone treatment merits further assessment in primary biliary cirrhosis over a longer period, with attention to selection of patients most likely to benefit and continuing observation of bone mass to better establish the "cost/benefit" ratio.
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PMID:A pilot, double-blind, controlled 1-year trial of prednisolone treatment in primary biliary cirrhosis: hepatic improvement but greater bone loss. 277 3

While people with type 1 diabetes mellitus (DM) often have bone deficiency, the relation between this deficiency and the duration or control of diabetes remains controversial. To assess the possibility of such an interrelationship, we studied parameters relating to mineral metabolism (Ca, P, alkaline phosphatase, Mg, PTH, and hydroxyproline (OHP)); bone remodeling (osteocalcin); diabetic control (HbA1c); and radiological study of the second metacarpal of the left hand and of bone age in 87 children with type 1 DM. The mineral parameters were not abnormal among the diabetics. Diabetic children had similar levels of fasting osteocalcin as normals (10.05 +/- 4.9 vs. 9.79 +/- 3.34 ng/ml, mean +/- SD); this did not differ by sex. The bone age fell within two standard deviations of the mean, and 9.5% of the diabetics had a bone mass deficit (less than the mean cortical thickness) greater than 2 SD. There was no correlation between osteocalcin and Ca, P, glycemia, HbA1c, PTH, Mg, or OHP. Our results do not support any association between bone mass loss and the severity or duration of type 1 diabetes. Bone turnover, measured by serum osteocalcin, was normal. Therefore the pathogenesis of osteopenia in type 1 DM remains unclear, and requires further investigation.
Diabetes Res Clin Pract 1989 Apr 01
PMID:Study of bone loss in diabetes mellitus type 1. 278 8


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