Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phosphatidylethanolamine N-methylation was studied in cardiac sarcolemma 8 weeks after the induction of chronic experimental diabetes in rats by a streptozotocin injection (65 mg/kg, iv). Incorporation of radiolabeled methyl groups from S-adenosyl-L-methionine into intramembranal phosphatidylethanolamine, assayed under optimal conditions, confirmed the existence of three catalytic sites involved in the sequential methyl transfer reactions. Total methyl group incorporation at all three sites was significantly depressed in diabetic myocardium, but this change was reversible by a 14-day insulin therapy to the diabetic animals. Measurements of phospholipid N-methylation activity at different times indicated that the depression was evident at 6 weeks after the induction of diabetes. This defect was also seen for the individual methylated lipid products (monomethyl-, dimethylphosphatidylethanolamine, and phosphatidylcholine) specifically formed at each catalytic site. Experiments with different concentrations of S-adenosyl-L-methionine revealed that, for all three sites, the apparent affinity for the methyl donor did not change, whereas the apparent Vmax values were significantly lowered in diabetes. The results of this study identify a defect in the sarcolemmal phosphatidylethanolamine N-methylation in diabetic cardiomyopathy.
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PMID:Sarcolemmal phosphatidylethanolamine N-methylation in diabetic cardiomyopathy. 647 54

Chronic streptozotocin-induced diabetes in rats was associated with a significant loss in the ability of isolated cardiac sarcolemmal membranes to bind Ca2+. Administration of insulin to the diabetic rats normalized the sarcolemmal Ca2+ binding capacity. The content of sialic acid residues, which are considered to represent a superficial Ca2+ pool in sarcolemma, was decreased in preparations from diabetic rats, and this change also was reversible upon insulin treatment of the diabetic rats. Treatment of sarcolemma with neuraminidase decreased Ca2+ binding by 37% in control preparations but had no effect on diabetic preparations. Diphosphatidylglycerol content was decreased but other acidic phospholipids such as phosphatidylinositol and phosphatidylserine, which also bind Ca2+, were not altered during diabetes. An increase in lysophosphatidylcholine and a decrease in phosphatidylethanolamine contents were observed in membranes isolated from diabetic rats. These results suggest that some alterations occur in Ca2+ binding and composition of heart sarcolemma in chronically diabetic rats and may provide further insight into the pathogenesis of diabetic cardiomyopathy.
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PMID:Alterations in Ca2+ binding by and composition of the cardiac sarcolemmal membrane in chronic diabetes. 657 35

The left ventricular systolic function of 32 patients with insulin-dependent diabetes mellitus was investigated by measurement of systolic time intervals. Patients with clinical signs of sclerosis in the coronary arteries were excluded. Twenty-nine sex- and age-matched healthy people served as controls. Resting values of PEP/LVET ratio and of the corrected pre-ejection period were significantly higher in diabetics than in controls. The alterations of systolic time intervals during volume-loading induced by passive leg-raising as well as by isometric handgrip test indicated an increase in left ventricular performance in healthy people. The unchanged systolic time intervals observed in diabetics during the same loadings indicated a decrease in the functional reserve of the diabetic left ventricle. The systolic time intervals observed in patients with type-1 diabetes could be evaluated as a preclinical abnormality of left ventricular performance and as early signs of diabetic cardiomyopathy.
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PMID:Preclinical abnormality of left ventricular performance in patients with insulin-dependent diabetes mellitus. 666 3

The effect of chronic experimental diabetes on the adenylate cyclase system (AC) in the rat heart was investigated. Rats were made diabetic by an intravenous injection of streptozotocin (65 mg/kg), hearts were removed 8 weeks later and washed cell particles were isolated. AC activity was measured in the absence and presence of different concentrations of forskolin, NaF, GTP analogue [Gpp(NH)p] or epinephrine. A significant depression in the epinephrine stimulated AC activity was observed in diabetic hearts. Basal AC activity and stimulation of AC with forskolin, NaF and Gpp(NH)p were not significantly different between control and diabetic preparations. These results indicate no apparent alterations in the regulatory or catalytic properties of AC in hearts from chronic diabetic rats. The observed depression in epinephrine stimulated AC activity may account for the depressed inotropic action of catecholamines in the diabetic cardiomyopathy.
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PMID:Alterations in adenylate cyclase activity due to streptozotocin-induced diabetic cardiomyopathy. 670 25

One feature of the diabetic cardiomyopathy is the appearance of contractile dysfunction as the workload increases. We hypothesized that this resulted from an impaired creatine kinase/phosphocreatine system and therefore examined the creatine kinase kinetics at both low and high workloads. Creatine kinase flux (by 31P nuclear magnetic resonance saturation transfer method), cardiac performance, and oxygen consumption were measured in control and streptozotocin-induced diabetic rat hearts. Creatine kinase flux was inhibited by iodoacetamide in control hearts to confirm the role of the creatine kinase/phosphocreatine system in cardiac performance. In diabetic hearts, 1) the contractile dysfunction became apparent only at high workloads, 2) the ATP synthesis rate was not significantly different from control hearts, 3) the creatine kinase flux was reduced by 30.8% (257.5 +/- 7.7 mumol.g wet wt-1.min-1 in control vs. 178.3 +/- 9.4 in diabetes, P < 0.001), and 4) the creatine kinase flux did not increase as the workload increased. In control hearts, 5) iodoacetamide inhibited the creatine kinase flux to the same degree as that in diabetic hearts, and 6) the contractile dysfunction was not as severe as that observed in diabetic hearts. These results suggest that the impaired creatine kinase/phosphocreatine system is, at least in part, responsible for the contractile dysfunction in the diabetic cardiomyopathy.
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PMID:Creatine kinase kinetics in diabetic cardiomyopathy. 761 80

Type I and type II diabetes is associated with increased cardiovascular complications, the most common of which are ischaemic cardiomyopathy and left ventricular dysfunction. The existence of an independent disease, diabetic cardiomyopathy, was suggested by initial anatomic studies, experimental models, and, more recently, by epidemiological studies. The exact cause of this ventricular dysfunction is not known: several mechanisms have been proposed, such as metabolic abnormalities of glucose transport, cellular overload in fatty acid metabolites, alteration of calcium uptake by the sarcoplasmic reticulum leading to cellular calcium overload, coronary microangiopathy, structural collagen abnormalities, interstitial and perivascular fibrosis or the presence of an autonomic neuropathy. The condition is characterised by abnormal left ventricular filling suggesting poor compliance or prolongation of left ventricular relaxation. Left ventricular systolic function is usually normal at rest but abnormally decreased on effort. The value of strict metabolic control and the place of drug therapy, especially calcium antagonists which oppose cellular calcium overload, has yet to be established. The natural history of diabetic cardiomyopathy should be defined by clinical studies taking care to differentiate it from the cardiovascular consequences of hypertension or obesity which aggravate or stimulate this condition.
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PMID:[Diabetic cardiomyopathy]. 764 66

The characteristic features of diabetic cardiomyopathy have been reported to be increased collagen formation associated with impairment of ventricular performance, based on experimental models of diabetes. The present study was therefore designed to clarify collagen gene expression in hearts obtained from female spontaneously diabetic BioBreeding Worcester Tokyo (BB/W@Tky) rats. Cardiac hypertrophy was observed as early as 14 weeks in diabetic BB/W@Tky rats, i.e. 4 weeks after the onset of diabetes. Left ventricular gene expression of collagen alpha 1 (I) was decreased to 10.6% of the control level. In 24-week-old diabetic rats, which had more marked cardiac hypertrophy, the level of alpha 1 Type I collagen mRNA was further decreased to 5.7% of the control level, whereas collagen alpha 1 (IV) mRNA demonstrated a 3-fold increase. As a result, a ratio of collagen alpha 1 (IV) to actin mRNA was positively correlated with plasma glucose concentration. These results suggest that hyperglycemia may alter the gene expression of extracellular matrix proteins, resulting in the morphological and functional changes seen in diabetic cardiomyopathy.
Diabetes Res Clin Pract 1994 Dec 31
PMID:Reciprocal changes in left ventricular collagen alpha 1 chain gene expression between types I and IV in spontaneously diabetic rats. 773 96

Diabetes mellitus induces microvascular damage within the myocardium, without coexistent changes in the extramural coronary arteries. Nonenzymatic glucosylation forms the biochemical basis of diabetic microangiopathy, which further causes specific structural changes of the heart muscle. These changes increase left ventricular stiffness and lead to diastolic filling abnormalities, that may be the first sign of diabetic cardiomyopathy. In this review the author discusses the pathogenesis of the microangiopathy of the heart in diabetes and the methods of its early detection.
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PMID:[Cardiac microangiopathy in diabetics]. 773 28

Heart failure, arrhythmia, or chest pain can be a consequence of diabetes independent of coronary disease or hypertension. Diastolic myocardial dysfunction is common, contributing to the high mortality during acute infarction. The authors discuss diabetic cardiomyopathy and its management.
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PMID:Diabetic cardiomyopathy: experimental and clinical observations. 780 91

Sixty-one children with insulin-dependent diabetes mellitus and twenty-three healthy subjects were investigated. The patients with diabetes mellitus aged 4 to 20 years (13.4 +/- 4.0) had had diabetes for 1 to 16 years (6.4 +/- 3.5). There were no cardiovascular risk factor other than diabetes. Patients received no medication other than insulin. The following echocardiographic and Doppler parameters of the left ventricle were analyzed in both groups: systolic and diastolic dimensions, systolic time intervals, fractional shortening, mean velocity of circumferential fiber shortening, percent relaxation of the left ventricular posterior wall at 50% of diastole, peak velocity of early (E) and late atrial (A) mitral flow. E/A ratio, deceleration of the E-wave, and the isovolumetric relaxation time. None of the parameters were significantly different between the groups. There was no relation observed between duration of diabetes and any of the parameters analyzed. It is concluded that there is not echocardiographic data to support the concept of diabetic cardiomyopathy in adolescents with type I (insulin-dependent) diabetes mellitus.
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PMID:Left ventricular function determined by Doppler echocardiography in adolescents with type I (insulin-dependent) diabetes mellitus. 783 62


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