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)

This study was made to determine whether zinc deficiency is one of the factors involved in growth retardation of infants of high-risk pregnancies. The high risk factors were hypertension of pregnancy, diabetes mellitus, congenital heart disease, chronic nephritis, rheumatic heart disease and hyperthyroidism. 102 neonatal infants were divided into 3 groups: breast fed group, 37 cases; test group, 32 cases formula-fed with supplementary zinc 1.14-2.28 mg/kg/d; and control group, 33 cases formula-fed and supplemented with Vitamin B complex as placebo. The groups were divided by double-blind and randomized method. There were no differences in the 3 groups in sex ratio, growth status and serum zinc concentration at the beginning of the study. Anthropometric data were obtained at 0, 3 and 6 months.
 ...
PMID:Growth promoting effect of zinc supplementation in infants of high-risk pregnancies. 129 Dec 3

Under the sponsorship of the National Institute on Aging and the National Institute of Diabetes and Digestive and Kidney Diseases, the Life Sciences Research Office of the Federation of American Societies for Experimental Biology held a workshop entitled, "The Role of Folate and Vitamin B-12 in Neurotransmitter Metabolism and Degenerative Neurological Changes Associated with Aging." The purpose of the May 1988 workshop was to bring together scientists from various disciplines to identify opportunities for research on an important topic relating to neuroscience, nutrition and aging.
 ...
PMID:The role of folate and vitamin B-12 in neurotransmitter metabolism and degenerative neurological changes associated with aging: proceedings of a workshop. 256 13

The effects of vitamin B6 on erythrocyte metabolism, erythrocyte hemoglobin O2 affinity (P50), and nonenzymatic glycosylation were studied in 15 Caucasian men with type II (non-insulin-dependent) diabetes mellitus. A control group of 13 healthy Caucasian men was also evaluated. Before treatment, diabetic subjects had low mean cell hemoglobin concentration values and increases in both erythrocyte 2,3-diphosphoglycerate (2,3-DPG) levels and erythrocyte hexokinase activities. Although all three of these changes are associated with a decrease in hemoglobin O2 (Hb-O2) affinity, P50 values were normal in diabetic subjects. Moreover, P50 values normalized to pH 7.4 (P50(7.4] were inversely related to the level of glycosylated hemoglobin (HbA1c). Both erythrocyte 2,3-DPG and erythrocyte ATP were also inversely related to HbA1c. Vitamin B6 nutriture, as determined by erythrocyte aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, was normal in all diabetic subjects before vitamin B6 therapy. Nonetheless, HbA1c levels decreased after 6 wk of treatment with 150 mg/day pyridoxine and increased again during placebo administration. These changes were not explained by changes in fasting blood glucose. Pyridoxine therapy also decreased P50(7.4) values and increased erythrocyte AST and ALT activities but had no effect on 2,3-DPG, ATP, or the activities of hexokinase, glucose-6-phosphate dehydrogenase, and 6-phosphogluconate dehydrogenase. These observations suggest that 1) nonenzymatic glycosylation may play a role in regulating both erythrocyte metabolism and Hb-O2 affinity in diabetic subjects, and 2) vitamin B6 therapy may modify nonenzymatic glycosylation of hemoglobin in this population.
Diabetes 1989 Jul
PMID:Erythrocyte O2 transport and metabolism and effects of vitamin B6 therapy in type II diabetes mellitus. 273 64

Pyridoxine binding to liver plasma membrane isolated from livers of normal and streptozotocin-induced diabetic rats was investigated. The effect of increasing concentration of pyridoxine on its binding to the membranes revealed a concentration-dependent and saturable process with a significant decrease in the high affinity receptor sites of the diabetic membrane. Moreover, the incubation of the membranes with procaine, colchicine and vincristine increased significantly pyridoxine binding to normal and diabetic membrane. Treatment of the normal and diabetic membranes with insulin did not affect pyridoxine binding. It could be suggested that streptozotocin-induced diabetes caused an alteration in the pyridoxine binding capacity of the liver plasma membrane which might be due to certain structural changes in the membrane.
 ...
PMID:Pyridoxine binding to normal and diabetic liver plasma membrane. 637 28

A study was undertaken to test the effect of pyridoxine supplementation on glucose tolerance in diabetes mellitus. Thirteen adult maturity-onset diabetics were studied. Seven were vitamin B6 deficient, as assessed by the stimulation of erythrocyte glutamic oxaloacetic transaminase in vitro by pyridoxal phosphate. All patients received pyridoxine hydrochloride (40 mg twice daily) for 3 weeks. Pyridoxine supplmentation did not bring about any significant alterations in either the oral glucose tolerance or the insulin response to glucose.
 ...
PMID:Failure of pyridoxine to improve glucose tolerance in diabetics. 718 14

Of 1017 patients admitted to the Royal Perth Hospital Diabetic Survey 142 were found to have significant bacteriuria. In these bacteriuric patients serum pyridoxal concentrations were significantly reduced (P = less than 0.001) when compared with 142 diabetic patients matched for age (+/- 5 years) and sex but without infection of the urinary tract. Measurements were repeated up to 6 mth after antibacterial treatment and serum pyridoxal concentrations were still low. Pyridoxal has a role in immunological competence, and it is possible that the increased incidence of urinary tract infection in patients with diabetes reflects impaired immunological competence due to pyridoxal deficiency.
 ...
PMID:The association of bacteriuria and reduced serum pyridoxal concentrations in patients with diabetes mellitus. 730 22

Vitamin B(6) (pyridoxine) supplementation has been found beneficial in preventing diabetic neuropathy and retinopathy, and the glycosylation of proteins. Oxygen radicals and oxidative damage have been implicated in the cellular dysfunction and complications of diabetes. This study was undertaken to test the hypothesis that pyridoxine (P) and pyridoxamine (PM) inhibit superoxide radical production, reduce lipid peroxidation and glycosylation, and increase the (Na+ + K+)-ATPase activity in high glucose-exposed red blood cells (RBC). Superoxide radical production was assessed by the reduction of cytochrome C by glucose in the presence and absence of P or PM in a cell-free buffered solution. To examine cellular effects, washed normal human RBC were treated with control and high glucose concentrations with and without P or PM. Both P and PM significantly lowered lipid peroxidation and glycated hemoglobin (HbA(1)) formation in high glucose-exposed RBC. P and PM significantly prevented the reduction in (Na+ + K+)-ATPase activity in high glucose-treated RBC. Thus, P or PM can inhibit oxygen radical production, which in turn prevents the lipid peroxidation, protein glycosylation, and (Na+ + K+)-ATPase activity reduction induced by the hyperglycemia. This study describes a new biochemical mechanism by which P or PM supplementation may delay or inhibit the development of complications in diabetes.
 ...
PMID:Pyridoxine and pyridoxamine inhibits superoxide radicals and prevents lipid peroxidation, protein glycosylation, and (Na+ + K+)-ATPase activity reduction in high glucose-treated human erythrocytes. 1116 69

The aim of this study was to investigate the relationship between total homocysteine levels in people with Type 2 diabetes and cognitive status. Fifty patients from our diabetes unit (30 females/20 males) with diabetes were enrolled. All patients had fasting blood samples taken for measurement of cardiovascular risk factors; total cholesterol and triglyceride concentrations and other lipid fractions (lipoprotein (a), low density lipoprotein (LDL-cholesterol), high density lipoprotein (HDL-cholesterol)), glucose, HbA(1c) and homocysteine. 24-h urine collection was used to measure creatinine clearance and microalbuminuria. Vitamin B-12 and folate were measured to assess vitamin status. All diabetic patients were assessed for late complications and a Mini-Mental State Examination (MMSE) was performed. The patients were 64.6 (49-78) years old with body mass index (BMI) of 29.6 +/- 6.3 kg/m(2), and duration of diabetes of 8.9 +/- 6.7 years. A univariant correlation analysis was performed among cardiovascular risk factors and vitamins with total MMSE score. Total homocysteine was inverse by correlated with MMSE score (r=-0.38; P<0.05) of the other measures of cardiovascular risk, microalbuminuria showed an inverse correlation with MMSE score (r=-0.51:P<0.01). Lipoproteins, glucose control and vitamin status were not correlated MMSE score. In the multiple regression model only microalbuminuria remained in the model, showing a decrease of one point in the MMSE result with each milligram of microalbuminuria, adjusted for confounding factors. Cognitive status in type 2 diabetic was correlated with homocysteine levels and microalbuminuria, this last endothelial damage marker remaining as an independent risk factor of cognitive deterioration.
Diabetes Res Clin Pract 2002 Mar
PMID:Total homocysteine and cognitive deterioration in people with type 2 diabetes. 1185 94

Advanced glycation end products (AGEs) from the Maillard reaction contribute to protein aging and the pathogenesis of age- and diabetes-associated complications. The alpha-dicarbonyl compound methylglyoxal (MG) is an important intermediate in AGE synthesis. Recent studies suggest that pyridoxamine inhibits formation of advanced glycation and lipoxidation products. We wanted to determine if pyridoxamine could inhibit MG-mediated Maillard reactions and thereby prevent AGE formation. When lens proteins were incubated with MG at 37 degrees C, pH 7.4, we found that pyridoxamine inhibits formation of methylglyoxal-derived AGEs concentration dependently. Pyridoxamine reduces MG levels in red blood cells and plasma and blocks formation of methylglyoxal-lysine dimer in plasma proteins from diabetic rats and it prevents pentosidine (an AGE derived from sugars) from forming in plasma proteins. Pyridoxamine also decreases formation of protein carbonyls and thiobarbituric-acid-reactive substances in plasma proteins from diabetic rats. Pyridoxamine treatment did not restore erythrocyte glutathione (which was reduced by almost half) in diabetic animals, but it enhanced erythrocyte glyoxalase I activity. We isolated a major product of the reaction between MG and pyridoxamine and identified it as methylglyoxal-pyridoxamine dimer. Our studies show that pyridoxamine reduces oxidative stress and AGE formation. We suspect that a direct interaction of pyridoxamine with MG partly accounts for AGE inhibition.
 ...
PMID:Effect of pyridoxamine on chemical modification of proteins by carbonyls in diabetic rats: characterization of a major product from the reaction of pyridoxamine and methylglyoxal. 1205 89

Pyridoxamine (PM), originally described as a post-Amadori inhibitor of formation of advanced glycation end-products (AGEs), also inhibits the formation of advanced lipoxidation end-products (ALEs) on protein during lipid peroxidation reactions. In addition to inhibition of AGE/ALE formation, PM has a strong lipid-lowering effect in streptozotocin (STZ)-induced diabetic and Zucker obese rats, and protects against the development of nephropathy in both animal models. PM also inhibits the development of retinopathy and neuropathy in the STZ-diabetic rat. Several products of reaction of PM with intermediates in lipid autoxidation have been identified in model reactions in vitro and in the urine of diabetic and obese rats, confirming the action of PM as an AGE/ALE inhibitor. PM appears to act by a mechanism analogous to that of AGE-breakers, by reaction with dicarbonyl intermediates in AGE/ALE formation. This review summarizes current knowledge on the mechanism of formation of AGE/ALEs, proposes a mechanism of action of PM, and summarizes the results of animal model studies on the use of PM for inhibiting AGE/ALE formation and development of complications of diabetes and hyperlipidemia.
 ...
PMID:Pyridoxamine, an inhibitor of advanced glycation and lipoxidation reactions: a novel therapy for treatment of diabetic complications. 1456 7


1 2 3 4 Next >>