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

The solubility of skin collagen into acetic acid and by pepsin digestion and the degree of non-enzymatic glycosylation of collagen (ketoamine linkage) in these fractions was determined in skin specimens from 27 insulin-dependent diabetic subjects and from 17 age-matched controls. Glycosylation in acid soluble collagen specimen was significantly increased in the diabetics, 1.9 +/- 1.8 (SD)ng of hexose/micrograms of hydroxyproline in comparison to the controls. 0.9 +/- 0.8 ng of hexose/micrograms of hydroxyproline. No significant difference in this respect was noted in pepsin soluble collagen specimens. The solubility of collagen into acetic acid and by pepsin digestion were significantly reduced in the diabetics. No clear relationships between non-enzymatic glycosylation or collagen solubility and diabetic late complications (nephropathy, retinopathy or limited joint mobility) were noted. We suggest (a) that equilibrium levels of early glycosylation products are different in acid and pepsin soluble collagen specimens. (b) ketoamine linkage glycosylation products by themselves are not directly involved in diabetic late complications and (c) the solubility in acid and digestibility of collagen by pepsin may be an indicator, even though nonspecific, of increased amounts of advanced glycosylation end products.
Diabetes Res 1989 Jul
PMID:Increased non-enzymatic glycosylation and reduced solubility of skin collagen in insulin-dependent diabetic patients. 262 62

Glycosylated haemoglobin (HbA1C) and serum protein bound hexose (SPBH) levels were estimated in 35 healthy control subjects and 35 diabetic subjects. The mean levels of SPBH in control subjects was 161.69 +/- 3.84 mg/dl. The SPBH levels in diabetic subjects were found to be increased (P less than 0.001). It was not influenced by age and sex of the patients, complications, type of diabetes and treatment received. HbA1C levels in control subjects were 5.33 +/- 0.38/dl. The HbA1C levels in diabetic subjects was found to be markedly elevated (11.95 +/- 0.46/dl) and was found to be highly significant (P less than 0.001). The levels were found to be on higher side in juvenile diabetics. A progressive linear correlation was observed between fasting blood sugar levels and concentration of SPBH and glycosylated haemoglobin concentration. A significant correlation was also observed between the levels of glycosylated haemoglobin and SPBH levels (P less than 0.05).
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PMID:Glycosylated haemoglobin(HbA1C) and serum protein bound hexose in diabetes mellitus. 207 32

We have examined polyol pathway kinetics in the lenses of rats made diabetic with streptozotocin. At up to 11 days after diabetes induction, the lenses were isolated and subjected to 'pulse-chase' studies: the lenses were incubated with [13C]glucose and lens metabolism followed by [13C]nuclear magnetic resonance (NMR) spectroscopy. Proton NMR spectroscopy was also performed to measure the hexose monophosphate shunt (HMPS) activity. The results showed that (1) the activity of aldose reductase increased initially and decreased after 11 days of diabetes; (2) the fructose pool increased initially but started to decline after 3 days; (3) the HMPS activity increased nearly 40% immediately after diabetes induction; and (4) the turnover rates of glucose, alpha-glycerophosphate (GP), lactate, sorbitol, and fructose were 80.8 +/- 2.6, 10.1 +/- 1.4, 47.7 +/- 3.7, 7.9 +/- 0.9 and 5.2 +/- 2.2 nmol hr-1 lens-1 (34 mg wet weight lens-1), respectively. Up to 35% of lactate appeared to derive from the polyol pathway. Further, GP was rapidly metabolized, although its fate is currently unknown. These results reveal a far more complex pattern of glucose metabolism in the diabetic lens than that in lenses incubated in high glucose.
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PMID:Polyol pathway activity in streptozotocin-diabetic rat lens. 275 93

1. Short term (1-2 hr) and long-term (2 days) effects of experimental alloxan induced diabetes on the kinetics of the renal hexose monophosphate shunt dehydrogenases are reported. 2. Alloxan diabetes for 2 days significantly increased kidney weight (16%) adding about 80 mg/day per g of kidney. No significant changes were found in renal growth 1-2 hr after alloxan injection. 3. Under these experimental conditions, the activities of glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase significantly increased (103 and 33% respectively) at all substrate concentrations, without affecting the KmS of either enzyme. 4. There was no effect of alloxan on the activity of these enzymes at 1-2 hr. Saturation curves show that all enzymes exhibited a M-M kinetic without evidence of sigmoidicity. 5. The results suggest that increased renal hexose monophosphate dehydrogenases activities are due to increased concentrations of the rate limiting proteins. 6. The relationship between these changes and renal hypertrophy is also discussed.
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PMID:Influence of experimental diabetes on the kinetic behaviour of renal cortex hexose monophosphate dehydrogenases. 279 53

Transport of the non-metabolizable hexose analogue 3-O-methyl-D-glucose (3OMG) was measured at 37 degrees C, pH 7.4, in human polymorphonuclear leukocytes (PMNLs) obtained from 15 ml of fresh venous blood. In the study, 0.05 mM of 3OMG was equilibrated with a half-time of about 10 s, and the rate constant was 0.074/s in PMNLs from a healthy subject (male, 38 years). The coefficient of variation of values assayed on different days was about 7% and the intra-assay variation was about 2%. The transport rate did not differ between the two sexes or between subjects of different ages (23-63 years), but was significantly higher in 23 patients with non-insulin-dependent diabetes than in 29 normal controls (13.3 +/- 3.7 vs. 10.4 +/- 2.5 fl/cell.s, mean +/- SD). In conclusion, the measurement of transport of 3OMG in PMNLs may be useful for the study of glucose transport in clinical investigations.
Diabetes Res Clin Pract 1989
PMID:Clinical application of measurement of glucose transport in human polymorphonuclear leukocytes. 280 56

In rat pancreatic islets, hypoxia severely decreased both the oxidation of D-[U-14C]glucose and the release of insulin evoked by D-glucose. The production of [14C]lactate was increased in the hypoxic islets, the relative magnitude of such an increment being greater at low (2.8 mM) than high (8.3 and 16.7 mM) D-glucose concentrations. Hypoxia increased the detritiation of D-[5-3H]glucose at low glucose concentration (2.8 mM), failed to affect 3H2O production at an intermediate glucose level (8.3 mM), and inhibited the utilization of D-[5-3H]glucose at a higher hexose concentration (16.7 mM). In tumoral islet cells (RINm5F line) exposed to 16.7 mM D-glucose, hypoxia decreased D-[U-14C]glucose oxidation to the same extent as in normal islet cells, but increased the production of [14C]lactate and 3H2O to a greater extent than in normal islets. These findings indicate that the Pasteur effect is operative in islet cells. The experimental data also suggest that, under normal conditions of oxygenation, high concentrations of D-glucose lead to both activation of phosphofructokinase and stimulation of mitochondrial oxidative events in normal, but not tumoral, islet cells.
Diabetes Res 1988 Feb
PMID:Hexose metabolism in pancreatic islets: the Pasteur effect. 284 Feb 31

Hearts isolated from non-insulin-dependent diabetic rats were found to exhibit reduced rates of basal and insulin-stimulated glucose metabolism. Since tissue levels of fructose 1,6-bisphosphate are significantly reduced in the diabetic heart, it was concluded that phosphofructokinase may be inhibited. However, neither glycogen nor glucose 6-phosphate accumulated in the myocyte, indicating that the phosphofructokinase reaction was not a bottleneck diverting substrate away from glycolysis. The other major factor contributing to decreased glycolytic flux in the diabetic heart is the impairment in glucose transport. Both basal and insulin-stimulated transport of 3-O-methyl-D-glucose was 30% less in the diabetic heart. While insulin sensitivity was unaltered in the diabetic rat, insulin responsiveness was decreased, indicating that the impairment in insulin-stimulated hexose transport was caused by a post-receptor defect. The net result of these abnormalities in glucose metabolism is a significant reduction in the rate of ATP synthesis by the diabetic heart.
Diabetes 1986 May
PMID:Postreceptor myocardial metabolic defect in a rat model of non-insulin-dependent diabetes mellitus. 293 76

The reduction of oxygen by the ene-diol tautomer of simple monosaccharides produces hydrogen peroxide and alpha-oxoaldehydes. This process, termed monosaccharide autoxidation, occurs at physiological pH and temperature and may contribute to the development of several pathological processes. Enolization of the monosaccharide to an ene-diol tautomer is a prerequisite for the reaction of the monosaccharides with oxygen. The reaction kinetics suggest a two step process: the enolization of the monosaccharide to the ene-diol followed by the reaction of the ene-diol with oxygen. Free-radical reactive intermediates are formed by the reaction of the ene-diol with oxygen: superoxide, semidione, and 1-hydroxyalkyl radicals are formed under physiological conditions (hydroxyl radicals are also detected at high pH). The autoxidation of monosaccharides stimulates the oxidation of oxyhemoglobin in erythrocytes, producing methemoglobin and hydrogen peroxide, and the oxidation of reduced pyridine nucleotides NAD(P)H to the oxidized congener NAD(P)+ and enzymatically inactive nucleotide. This stimulates oxidative metabolism (via the hexose monophosphate shunt) and alpha-oxoaldehyde metabolism (via the glyoxalase system) in erythrocytes in vitro. The oxidative challenge is relatively mild even with very high concentrations (50 mM) of monosaccharide. However, crosslinking of membrane proteins by alpha-oxoaldehydes is enhanced; this effect may exacerbate ageing and decrease the lifetime of erythrocytes in circulation. In vivo, the autoxidation of monosaccharides is expected to be a chronic oxidative process occurring in biological tissue which utilises simple monosaccharides, e.g., in glycolysis and gluconeogenesis. Monosaccharide autoxidation is suggested to be a determinant in the control of cellular mitosis and ageing, providing physiological substrates for the glyoxalase system, and may contribute to the chronic disease processes associated with diabetes mellitus and the smoking of tobacco.
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PMID:Monosaccharide autoxidation in health and disease. 300 96

Diabetes mellitus is marked by hyperglycemia and a variety of other metabolic disorders. The significance of hyperglycemia in the pathogenesis of diabetic retinopathy has proven difficult to evaluate in patients. Diabetic dogs are known to develop retinal lesions morphologically identical to those typical of diabetes in man, provided hyperglycemia in the animal is allowed to persist at least for many months and usually for 3 to 5 years. The development of retinopathy in this animal model can be inhibited by careful improvement of diabetic (glycemic) control. Comparable retinopathy has recently been found to develop in nondiabetic dogs as a result of experimental galactosemia of several years' duration. Included in this retinopathy and in the retinopathy of diabetic patients and dogs as well are saccular capillary aneurysms, hemorrhages, nonperfused or acellular vessels, varicose vessels, and loss of capillary pericytes. Retinal capillary basement membrane has been measured (to date) in two dogs that had been galactosemic for 5 years, and it was found to be significantly thicker than in normal dogs (P less than 0.01). Many metabolic abnormalities typical of diabetes are absent from galactosemic dogs. Unlike diabetic dogs, the blood levels of glucose, nonesterified fatty acids, branched-chain amino acids, and fibrinogen are not elevated in the galactosemic dogs, and their serum insulin concentration seems normal. Excessive blood hexose itself appears to be an important determinant of retinopathy. One possible mechanism by which excessive blood hexose might produce retinopathy involves the polyol pathway.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperglycemia as a cause of diabetic retinopathy. 308 5

A competitive ELISA for quantitative determination of glucitollysine, the reduced hexose alcohol form of glucose conjugated to the epsilon amino group of lysine was developed. We applied it to measure non-enzymatically glycated serum proteins. The antiserum obtained by immunizing guinea pigs with reductively glycated human albumin was capable of identifying and quantitating glucitollysine residues of serum proteins in normal and diabetic subjects after reduction of the proteins with sodium borohydride. The ELISA assay developed here had satisfactory reproducibility as judged by the intra-assay precision of 2.3-7.6% and the interassay precision of 6.7-9.8%. Results from this assay procedure correlated well with those from the radioimmunoassay and the boronate affinity chromatography procedure. The data suggested that diabetic serum proteins contained at least three times as much immunochemically detectable glucitollysine residues as normal serum proteins after reduction of the proteins with sodium borohydride. This method allows to quantitate glucitollysine residues on any of the proteins that have been implicated in the pathological sequelae of diabetes.
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PMID:Quantitative enzyme-linked immunosorbent assay (ELISA) for non-enzymatically glycated serum protein. 310 4


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