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

It has been reported that lactate dehydrogenase virus (LDV) selectively infects a subpopulation of macrophages, thereby affecting the immune system. We studied the effects of LDV infection on the development of diabetes in non-obese diabetic (NOD) mice. Five-week-old female NOD mice were infected with LDV (10(8) ID50/mouse) and observed until 23 weeks of age. None of the 21-LDV-infected mice developed diabetes, whereas 10/14 (71.4%) uninfected mice did. Although the subpopulations of T cells and the percentage of Mac1-positive cells in the NOD murine spleen and the number of harvested peritoneal macrophages were unaffected by LDV infection, the proportions of Ia-positive peritoneal macrophages were significantly decreased in LDV-infected compared with uninfected mice (1.1 +/- 0.2%, 6.5 +/- 2.9%; P < 0.01). In LDV-infected NOD mice, insulitis of the same grade as that seen in uninfected NOD mice was observed. In another experiment, 3, 5, 10 or 16-week-old female NOD mice were infected with LDV. None of the mice infected with LDV at 3, 5 or 10 weeks of age developed diabetes and only one of six infected at 16 weeks of age did. These findings indicate that LDV infection suppresses the development of diabetes in female NOD mice by reducing the capacity of Ia-positive macrophages, and suggest that the development of human type 1 diabetes may be suppressed by certain viral infections.
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PMID:Suppression of development of diabetes in NOD mice by lactate dehydrogenase virus infection. 148 82

Na-K ATPase activity in the brain decreased significantly after diabetes was induced with streptozotocin in rats. Largest decreases were observed in the hippocampus (-30%) and the cerebral cortex (-26%). Smaller decreases were observed in the thalamus (-13%), hypothalamus (-11%) and brain stem (-10%). Na-K ATPase activity in the striatum and the cerebellum were not significantly decreased. The varied decreases suggest that the regional variation of the enzyme is enhanced in the diabetic state. The enzymes of glucose metabolic pathway, namely hexokinase, lactate dehydrogenase and citrate synthase in the brain regions largely remained unchanged although increases in lactate dehydrogenase were observed in some regions. Acetylcholinesterase activity, a marker for the cholinergic system, remains unaltered in the brain during diabetes. The results are discussed with respect to the possible metabolic factors which alter the Na-K ATPase in the brain and its comparison with the peripheral nerve.
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PMID:Diabetes induced by streptozotocin causes reduced Na-K ATPase in the brain. 166 46

With metabolically active, saponin-permeabilized adipocytes, in situ pathway metabolism, which was distal to glucose transport, was examined in acute streptozocin-induced diabetic (STZ-D) rats. Metabolic reactions were initiated with selectively radiolabeled glucose-6-phosphate (G6P), an otherwise inert substrate with intact cells. Thus, the membrane pores permitted a direct comparison of cellular flux between control and STZ-D adipocytes at identical initial substrate concentrations. Three metabolic pathways were studied: 1) proximal glycolysis through the triosephosphates ([3-3H]G6P to 3H2O), 2) glycolysis-Krebs ([6-14C]G6P) oxidation, and 3) lipogenesis ([6-14C]G6P incorporation into triglyceride). The extent of membrane porosity was assessed by both propidium iodide staining and lactate dehydrogenase leakage to assure that porosity was comparable between the cell groups. Porous adipocytes from STZ-D rats had markedly attenuated rates of G6P metabolism compared with controls. At enzyme-saturating concentrations of G6P (4 mM), this deficit ranged from 44% for glycolysis-Krebs oxidation to 88% for lipogenesis. The reduction in glycolysis-Krebs oxidation was also evident between 0.5 and 6 mM G6P. These porous-cell data were compared with parallel studies of glucose metabolism and clearance in intact adipocytes. Finally, several glycolytic enzymes and acetyl-CoA carboxylase were measured in cell-free (sonicated) extracts with traditional in vitro methods under Vmax conditions. Overall, the in situ porous-cell flux measurements uncovered larger deficits in posttransport cellular metabolism than were apparent in the cell-free, in vitro assays. We conclude that, in actively metabolizing porous rat adipocytes, there exists a striking and unequivocal transport-independent defect in intermediary metabolism after acute STZ-D.
Diabetes 1991 Nov
PMID:Diminished in situ glucose-6-phosphate flux in permeabilized adipocytes from streptozocin-induced diabetic rats. 183 3

Adult rats injected with streptozotocin during the neonatal period displayed in the fed state moderate hyperglycemia. However, the percentages of glycated hemoglobin in erythrocytes and glycated lactate dehydrogenase in liver and pancreatic islets, as well as the sorbitol and glycogen content of the islets, were not significantly increased. Likewise, in intact islets, the ouabain-sensitive inflow of 86Rb+, and the ratio between 3H2O production from D-[2-3H]glucose and D-[5-3H]glucose were not different in control and streptozotocin-injected rats. These findings suggest that the alteration in both the mitochondrial catabolism of D-glucose and secretory response to the hexose previously documented in the islets of the latter animals are not attributable to factors such as the excessive nonenzymatic glycation of cytosolic proteins, sorbitol or glycogen accumulation, or impaired Na+, K(+)-adenosine triphosphatase (ATPase) activity. Although a contributive role of glucotoxicity in the impaired function of beta cell in this model of non-insulin-dependent diabetes should not be ruled out, it is speculated that streptozotocin might also cause a long-term damage of key mitochondrial dehydrogenases in the pancreatic beta cells and, possibly, their precursor cells.
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PMID:Neonatal streptozotocin injection: a model of glucotoxicity? 183 15

Biochemical alterations in the hearts of non-diabetic and 5 weeks of streptozotocin-induced diabetic rats following isoproterenol (ISO) administration were compared. Serum lactate dehydrogenase (LDH) and myocardial adenosine triphosphate (ATP), creatine phosphate (CP), lactate and glycogen were used as indices of myocardial injury. Hearts from diabetic rats (blood glucose greater than 350 mg/dl), before ISO administration, had normal lactate levels but significantly low high-energy phosphate (HEP) levels and high glycogen levels in comparison to non-diabetic rats. No difference was observed in serum LDH levels between these two groups. ISO administration to non-diabetic rats caused myocardial necrosis as evidenced by a significant depletion of myocardial glycogen and HEPs along with significant myocardial lactate accumulation and an increase in serum LDH. However, the hearts from diabetic rats failed to show any significant HEP depletion, accumulation of lactate and leakage of LDH into serum following ISO-administration, though myocardial glycogen level was significantly lowered. These observations, in conjunction with earlier reports, point to the hypothesis that, in diabetes, there are certain alterations in the sarcolemma which hamper the process by which ISO causes myocardial necrosis.
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PMID:Isoproterenol fails to produce myocardial necrosis in streptozotocin-induced diabetic rats. 183 21

The effect of media conditioned by concanavalin A-activated spleen cells (C-sup) on insulin release and its islet cell cytotoxicity were studied. In a functional study, C-sup significantly inhibited both basal insulin release and glucose-stimulated insulin release. Morphologically, C-sup had a destructive effect on isolated islets after 72 h incubation. Islet cell cytotoxicity was shown by lactate dehydrogenase (LDH) release assay after 5 days incubation with C-sup in a dose-dependent manner. These results suggest that acceleration of the onset of diabetes in young diabetes prone (DP) Bio-Breeding/Worcester (BB/W) rats following the injection of C-sup may depend on the suppressive and cytotoxic effects of C-sup on pancreatic islet cells.
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PMID:Effect of media conditioned by concanavalin A activated spleen cells on pancreatic islet cells. 191 13

Data were obtained and analyzed in 229 patients admitted to the coronary care unit from November 1988 through July 1989. The patients were classified into 2 groups: patients without or with only mild left ventricular failure (Killip class I or II) during their hospital stay (group I), and patients who were in Killip class I or II on admission but developed cardiogenic shock during hospitalization (group II). Discriminant function analysis was performed using the following variables: patients' age, history of previous myocardial infarction, diabetes mellitus, blood lactate, urea, creatinine, creatine kinase, aspartate aminotransferase, lactate dehydrogenase concentrations, and chest x-ray cardiothoracic ratio. Variables that were found to significantly discriminate the 2 groups of patients were age, previous infarction, x-ray cardiothoracic ratio, blood urea and lactate concentrations. The risk index was computed, and blood lactate was the variable with the greatest predictive power for shock development. The sensitivity, specificity and predictive value of the risk index, taking various cutoff points, were calculated. With a cutoff value of 1, sensitivity was 65%, specificity 91%, positive predictive value 36% and negative predictive value 97%. With a cutoff value of 2, sensitivity was 53%, specificity 99%, positive predictive value 82% and negative predictive value 96%.
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PMID:Usefulness of blood lactate as a predictor of shock development in acute myocardial infarction. 200 Jul 87

All reported clinical characteristics of acute retroviral illness with the human immunodeficiency virus (HIV) are nonspecific. Signs and symptoms described are associated with a variety of acute infections. We report the cases of three patients in whom the acute retroviral illness was characterized by transient oral candidiasis and unexplained high lactate dehydrogenase values, with or without transient pulmonary infiltrate, in the context of an acute febrile illness. The clinical findings correlated with a severe reduction in the number of CD4 cells. We believe that thrush could be a marker of acute retroviral infection, as it is not a feature of any other heterophil-negative mononucleosis-like syndrome. We propose that in any patient having transient thrush and acute viral syndrome, the possibility of HIV infection should be aggressively pursued serologically, regardless of the patient's HIV risk status, provided that the usual causes of candidiasis (eg, diabetes mellitus, antibiotic use, and dentures) can be excluded.
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PMID:Oral candidiasis as a marker of acute retroviral illness. 205 63

The mean values of body mass index, haemoglobin A1, serum protein, total lipids, triglycerides, lactate dehydrogenase, alkaline phosphatase, amylase and beta-glucuronidase and heart rate and blood pressure and blood urea levels of Libyan diabetic patients with secondary complications are significantly higher than those of the patients without secondary complications. However, the mean values of fasting blood glucose, serum cholesterol and beta-N-acetylglucosaminidase of patients without complications are higher than those of the patients with secondary complications. The duration of diabetes in patients with secondary complications was 10.2 +/- 1 years while that of patients without complications was 5.2 +/- 0.65 years. The significance of these results is discussed.
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PMID:Secondary diabetic complications and biochemical parameters. 209 82

The phosphorylation of D-glucose, as catalyzed by liver postmicrosomal supernatants, prepared from diabetic rats, under conditions aiming at the characterization of gluco-kinase activity, indicates, in addition to the classical fall in enzyme activity, an altered kinetic behaviour, the affinity for D-glucose and the apparent energy of activation being both lower in diabetic than normal rats. These kinetic anomalies persist after separation of cytosolic proteins from low molecular weight metabolites by gel filtration chromatography. They are simulated, to a limited extent, when liver cytosolic proteins from normal rats are glycated in vitro through prolonged exposure to a high concentration of D-glucose. Diabetes causes an increased non-enzymatic glycation of liver cytosolic proteins, including lactate dehydrogenase, as judged by either the ketoamine test, a back-titration procedure or the separation of glycated proteins by affinity chromatography. These findings suggest that chronic hyperglycemia might alter the intrinsic properties of liver glucokinase through a process of non-enzymatic glycation.
Diabetes Res 1990 Jul
PMID:Kinetic behaviour of liver glucokinase in diabetes. II. Possible role of non-enzymatic protein glycation. 213 81


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