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

The insulin-like activity of bis-glycinato oxovanadium (IV) complex on experimental diabetes has been studied. Rats made diabetic with streptozotocin, after one month, were fed ad libitum with bis-glycinato oxovanadium (IV) complex (30 mg/100 ml) for fifteen days. The altered blood glucose, urea, cholesterol, triglycerides, liver glycogen and the activities of liver enzymes such as hexokinase, lactate dehydrogenase and fructose-1, 6-bisphosphatase, were reverted to normal levels in bis-glycinato oxovanadium (IV) complex treated diabetic rats, thereby suggesting for the insulin-mimetic effect of bis-glycinato oxovanadium (IV) in experimental diabetes.
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PMID:Insulin-like effects of bis-glycinato oxovanadium (IV) complex on experimental diabetic rats. 850 29

Left ventricular hypertrophy is considered to be an independent risk factor giving rise to ischemia, arrhythmias, and left ventricular dysfunction. Slow movement of intracellular calcium contributes to the impaired contraction and relaxation function of hypertrophied myocardium. Myofibril content may also be shifted to fetal-type isoforms with decreased contraction and relaxation properties in left ventricular hypertrophy. Myocyte hypertrophy and interstitial fibrosis are regulated independently by mechanical and neurohumoral mechanisms. In severely hypertrophied myocardium, capillary density is reduced, the diffusion distance for oxygen, nutrients, and metabolites is increased, and the ratio of energy-production sites to energy-consumption sites is decreased. The metabolic state of severely hypertrophied myocardium is anaerobic, as indicated by the shift of lactate dehydrogenase marker enzymes. Therefore, the hypertrophied myocardium is more vulnerable to ischemic events. As a compensatory response to severe cardiac hypertrophy and congestive heart failure, the ADP/ATP carrier is activated and atrial natriuretic peptide is released to increase high-energy phosphate production and reduce cardiac energy consumption by vasodilation and sodium and fluid elimination. However, in severely hypertrophied and failing myocardium, vasoconstrictor and sodium- and fluid-retaining factors, such as the renin-angiotensin system, aldosterone, and sympathetic nerve activity, play an overwhelming role. Angiotensin-converting enzyme inhibitors (ACEIs) are able to prevent cardiac hypertrophy and improve cardiac function and metabolism. Under experimental conditions, these beneficial effects can be ascribed mainly to bradykinin potentiation, although a contribution of the ACEI-induced angiotensin II reduction cannot be excluded.
Diabetes 1996 Jan
PMID:Substrate metabolism, hormone interaction, and angiotensin-converting enzyme inhibitors in left ventricular hypertrophy. 852 2

Lactate dehydrogenase (L-lactate : NAD+ oxidoreductase, EC 1.1.1.27) activity has been measured on the subpopulations of platelets obtained from blood of diabetic patients. Small, but not large platelets show a lactate dehydrogenase activity higher than that of controls. Moreover, a positive statistically significant correlation was found between the activity of small platelets and the percent of glycated haemoglobin, while no correlation was obtained in the case of large platelets. Since we previously demonstrated that lactate dehydrogenase activity of small platelets is exceedingly high in some clinical and experimental conditions, our results not only confirm the involvement of platelets in diabetes but provide more evidence in support of our previous hypothesis of a relationship between lactate dehydrogenase and in-vivo platelet activation.
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PMID:Lactate dehydrogenase activity of platelets in diabetes mellitus. 854 31

Special features of glucose metabolism in pancreatic beta-cells are central to an understanding of the physiological role of these cells in glucose homeostasis. Several of these characteristics are emphasized: a high-capacity system for glucose transport; glucose phosphorylation by the high-Km glucokinase (GK), which is rate-limiting for glucose metabolism and determines physiologically the glucose dependency curves of many processes in beta-cell intermediary and energy metabolism and of insulin release and is therefore viewed as glucose sensor; remarkably low activity of lactate dehydrogenase and the presence of effective hydrogen shuttles to allow virtually quantitative oxidation of glycolytic NADH; the near absence of glycogen and fatty acid synthesis and of gluconeogenesis, such that intermediary metabolism is primarily catabolic; a crucial role of mitochondrial processes, including the citric acid cycle, electron transport, and oxidative phosphorylation with FoF1 ATPase governing the glucose-dependent increase of the ATP mass-action ratio; a Ca(2+)-independent glucose-induced respiratory burst and increased ATP production in beta-cells as striking manifestations of crucial mitochondrial reactions; control of the membrane potential by the mass-action ratio of ATP and voltage-dependent Ca2+ influx as signal for insulin release; accumulation of malonyl-CoA, acyl-CoA, and diacylglycerol as essential or auxiliary metabolic coupling factors; and amplification of the adenine nucleotide, lipid-related, and Ca2+ signals to recruit many auxiliary processes to maximize insulin biosynthesis and release. The biochemical design also suggests certain candidate diabetes genes related to fuel metabolism: low-activity and low-stability GK mutants that explain in part the maturity-onset diabetes of the young (MODY) phenotype in humans and mitochondrial DNA mutations of FoF1 ATPase components thought to cause late-onset diabetes in BHEcdb rats. These two examples are chosen to illustrate that metabolic reactions with high control strength participating in beta-cell energy metabolism and generating coupling factors and intracellular signals are steps with great susceptibility to genetic, environmental, and pharmacological influences. Glucose metabolism of beta-cells also controls, in addition to insulin secretion and insulin biosynthesis, an adaptive response to excessive fuel loads and may increase the beta-cell mass by hypertrophy, hyperplasia, and neogenesis. It is probable that this adaptive response is compromised in diabetes because of the GK or ATPase mutants that are highlighted here. A comprehensive knowledge of beta-cell intermediary and energy metabolism is therefore the foundation for understanding the role of these cells in fuel homeostasis and in the pathogenesis of the most prevalent metabolic disease, diabetes.
Diabetes 1996 Feb
PMID:Banting Lecture 1995. A lesson in metabolic regulation inspired by the glucokinase glucose sensor paradigm. 854 69

Abnormalities of left ventricular function are often present in patients with diabetes who are in a stable metabolic state. To determine whether acute metabolic abnormalities may contribute to pathogenesis, patients with diabetes and ketoacidosis (Group 1) or hyperglycemia without ketosis (Group 2) were studied. They were assessed noninvasively for evidence of acute injury or dysfunction of the myocardium. Left ventricular function was assessed on admission and after clinical recovery. Myocardial enzyme release was examined during the acute phase. In Group 1, plasma glucose averaged 32 mM/L and carbon dioxide content 12.4 mEq/L. On echocardiography, the initial circumferential shortening velocity of 1.85 + 0.07 circumferences per second was significantly higher than the final circumferential shortening velocity of 1.31 + 01 (P < 0.005). The systolic time interval ratio, pre-ejection period/left ventricular ejection time, was significantly lower on the initial day compared with the second study. These data are consistent with enhanced ventricular performance. In group 2, plasma glucose averaged 29 mM/L, and carbon dioxide content was normal. The initial circumferential shortening velocity of 1. 1 circumferences per second and pre-ejection period/left ventricular ejection time ratio of 0.38 were normal and remained unchanged. There was no significant alteration of heart rate or arterial pressure in either group. In both groups, total serum lactate dehydrogenase and creatinine phosphokinase levels, as well as their cardiac isoenzymes, were within normal limits. Therefore, the initial increase of myocardial performance and subsequent restoration to normal, as well as the lack of cardiac enzyme increase in plasma, support the view that shortterm ketoacidosis does not contribute to the abnormalities of ventricular function in diabetes.
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PMID:Effect of acute ketoacidosis on the myocardium in diabetes. 861 75

A 38 year-old man with a 12-year history of noninsulin-dependent diabetes mellitus with rapidly progressive diabetic complications presented with microangiopathic hemolytic anemia and thrombocytopenia. He had no disorders that could induce microangiopathic hemolytic anemia other than diabetic microangiopathy. In addition, there was a significant negative correlation between serum lactate dehydrogenase levels and peripheral platelet counts, which suggested that the hemolysis and thrombocytopenia occurred through the same mechanism. Activated partial thromboplastin time was slightly prolonged, and lupus anticoagulant and antiphospholipid immunoglobulin G antibodies were positive. Both the hemolysis and the thrombocytopenia spontaneously improved after the initiation of hemodialysis. This is a unique case of diabetic microangiopathic hemolytic anemia and thrombocytopenia in which antiphospholipid syndrome also may be involved.
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PMID:Case report: diabetic microangiopathic hemolytic anemia and thrombocytopenia with antiphospholipid syndrome. 861 92

The effect of R, S, and racemic forms of a-lipoic acid was tested on the formation of opacity in normal rat lenses incubated with 55.6 mM glucose, as a model for in vivo diabetic cataractogenesis. Control lenses, incubated 8 days with 5.56 mM glucose, did not develop opacities. Formation of lens opacities in vitro was correlated with lactate dehydrogenase (LDH) leakage into the incubation medium. Opacity formation and LDH leakage, resulting from incubation in medium containing 55.6 mM glucose to model diabetes, were both suppressed by the addition of 1 mM R-lipoic acid. Addition of 1 mM racemic lipoic acid reduces these damaging effects to the lens by one-half, while S-lipoic acid potentiated LDH leakage, consistent with the hypothesis that R-lipoic acid is the active form. Although HPLC analysis demonstrated that both stereoisomers of lipoic acid were reduced to dihydrolipoate at comparable rates by the intact lens, the mitochondrial lipoamide dehydrogenase system is highly specific for reduction of exogenous R-lipoic to dihydrolipoic acid. Therefore, stereospecific protection against this opacity is consistent with specific reduction of R-lipoic acid in mitochondria of the vulnerable cells at the lens equator where the first globular degeneration is seen in glucose cataract.
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PMID:Modelling cortical cataractogenesis 17: in vitro effect of a-lipoic acid on glucose-induced lens membrane damage, a model of diabetic cataractogenesis. 867 20

We report a case of diabetic ketoacidosis (DKA) complicated by acute myocarditis, which was confirmed by cardiac biopsy. A 26-year-old man was hospitalized with severe DKA. On admission, nonspecific ST-T change was noted on the electrocardiogram (ECG). The patient's levels of creatine phosphokinase (CPK) and glutamic oxaloacetic transaminase were slightly elevated, but he did not complain of chest discomfort or symptoms of heart disease. On the first day after admission, ST-T elevation was noted on ECG during treatment of DKA. By cardiac angiography and cardiac biopsy, coronary heart disease was ruled out and postmyocarditic change was histologically confirmed. An episode of upper respiratory viral infection before the onset of acute diabetes suggested that the patient suffered from viral-induced myocarditis and consequent development of IDDM. This possibility was confirmed by the clinical course of ECG change, with elevated CPK and lactate dehydrogenase and a slightly elevated antibody titer for echovirus.
Diabetes Care 1996 Apr
PMID:A case of myocarditis associated with IDDM. 872 64

We have previously shown that the intramural motor nerves in the rat bladder can function in anoxic conditions. The present study aims to explore the distribution and activity of lactate dehydrogenase (LDH), the key enzyme for ATP generation in anoxia. The activity and isoform distribution pattern of LDH was studied in pelvic ganglia from male and female rats. A histochemical investigation showed that the LDH activity was intense in the ganglion cells, and weak in the other tissue components (nerve bundles, connective tissue). The male pelvic ganglion weighted 55% more than the female pelvic ganglion, the enzyme activity per unit ganglion weight was 60% higher and the total LDH activity was 155% higher. The isoform distribution was similar, with M4 being dominant isoform, followed by M3H. Infravesical outlet obstruction in the female rat induced a threefold increase in ganglion weight, and the total LDH activity increased twofold. In this hypertrophic female ganglion a decreased relative amount of M4, and an increased amount of MH3, was found. Diabetes in the male rat had no effect on ganglion weight or its contents and isoform distribution of LDH.
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PMID:Lactate dehydrogenase activity and isoform distribution in the rat pelvic ganglion: effects of diabetes and bladder outlet obstruction. 878 79

We investigated whether low density lipoprotein (LDL) under oxidative stress might induce the release of fructose, glucose-6-phosphate and fructose-6-phosphate from perivascular cells, and also whether these substances might accelerate the formation of advanced glycation end products (AGE) from proteins in vitro. When vascular smooth muscle cells were incubated with LDL in Ham's F10 at 37 degrees C for 48 h. release of all these substances was increased dose-dependently by oxidized LDL. Fructose release was increased in a dose-dependent manner by glucose. Indomethacin (20 microM) significantly (P < 0.01) suppressed the release of fructose (25.4 +/- 15.7% of control) and hexose phosphates (29.4 +/- 4.0) with the inhibition of release of lactate dehydrogenase (35.5 +/- 4.9) as well as probucol, whereas an aldose reductase inhibitor, epalrestat, significantly (P < 0.001) inhibited only the fructose release (0.9 +/- 0.8). Release of fructose and hexose phosphates from vascular endothelial cells was also induced by oxidized LDL. AGE immunoreactivities and AGE-related fluorescence formed from proteins and glucose were significantly increased (P < 0.001) in the presence of small amounts of the cellular glucose metabolites (6.6%) with glucose (93.4%). These data suggest that release of potent AGE initiators, fructose and hexose phosphates, from perivascular cells induced by oxidized LDL may be an important phenomenon for vascular complications.
Diabetes Res Clin Pract 1996 Mar
PMID:Release of fructose and hexose phosphates from perivascular cells induced by low density lipoprotein and acceleration of protein glycation in vitro. 879 96


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