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)

We report unusually high concentrations of free fatty acids and glycerol in sera of patients with adult-onset diabetes, and the accompanying alterations in creatine kinase isoenzyme MM patterns associated with such patients. The serum samples with increased free fatty acids also showed increased electrophoretic movement of the MM isoenzyme on cellulose acetate membranes. Fatty acid concentrations found in such samples averaged 9.88 +/- 5.65 (SD) meq/L and the average glycerol concentration was 153 +/- 115 (SD) mg/L. The serum glycerol concentrations correlated with those of the free fatty acids (r = 0.886, slope = 0.309, intercept = 4.76).
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PMID:Increased concentrations of free fatty acids and glycerol and altered creatine kinase MM isoenzyme patterns in certain diabetic patients. 46 58

Myocardial infarct extension after the acute event was defined as a second reise in the myocardial isoenzyme of serum creatine kinase (CK-B) after the initial return of CK-B to normal values. In 43 patients with acute myocardial infarcts, CK-B was measured by radioimmunoassay every 12 hours for 14 days. Nineteen patients had anterior transmural myocardial infarcts AMI, 14 had inferior transmural myocardial infarcts (IMI) and 10 had subendocardial myocardial infarcts (SEMI). Infarct extension as detectd by a second rise in serum CK-B occurred in six patients (32%) with AMI, two (14%) with IMI and two (20%) with SEMI; these differences are not statistically significant. Infarct extension for all patients combined was 23%. Four patients with AMI also had infarct extension as determined by recurrent chest pain. ECG alterations and other enzyme changes. In the other six, the infarct extension was undetected clinically. Four patients with AMI and infarct extension died within 3 weeks after hospitalization. We did not note any additional morbidity or mortality in patients with infarct extension who had IMI or SEMI. There was no significant difference in the frequency of previous myocardial infarction, history of hypertension, diabetes mellitus or smoking history in patients with and without infarct extension shown by serum CK-B isoenzyme elevations. The measurement of serum CK-B values with a quantitative and sensitive assay suggests that myocardial infarct extension occurs more commonly than clinically recognized, but the frequency of extension may be less than that reported in patients in whom precordial mapping and total serum CK values were measured to identify this phenomenon.
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PMID:Detection of myocardial infarct extension by CK-B radioimmunoassay. 75 95

Case 1, a 60-year-old man and case 2, a 70-year-old man had several year history of chronic renal failure with hypertension and hyperlipidemia due to diabetes mellitus. Treatment of hyperlipidemia was started by oral bezafibrate intake 1,200 mg per day in case 1 and 400 mg per day in case 2 respectively. Three to fourteen days later, both patients noticed symmetrical muscle pain and weakness. Then the symptoms worsened and they were hospitalized. At the time of admission, both patients revealed weakness in the proximal muscles of their upper and lower limbs and the serum creatine kinase and myoglobin levels were remarkably elevated. Myoglobinuria was also noted. Routine light microscopic examination of biopsied quadriceps femoris muscles of two patients showed scattered necrotic muscle fibers, some of which were under phagocytosis. The symptoms of the patients were immediately resolved after the drug was discontinued. Serum concentration of bezafibrate was remarkably elevated during treatment. Thus the diagnosis was established as having bezafibrate induced myopathy and, as far as we know, this is the first report of bezafibrate induced myopathy in Japan. On the basis of the above description, bezafibrate may induce muscle damage if dose is excess over the renal capacity. Extreme caution is warranted when the patient is placed on bezafibrate and has renal dysfunction. Strict dose adjustment is necessary in taking account of renal function to avoid muscle damage including rhabdomyolysis.
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PMID:[Bezafibrate myopathy in two patients with chronic renal failure]. 129 Nov 64

The effect of physical training on total creatine kinase (CK), CK-MM, and CK-MB isoenzyme activity was studied in hearts of diabetic and control rats. Diabetes was induced with streptozotocin (50 mg/kg), and only rats with blood glucose levels between 14 and 22 mmol/L 1 week later were kept in the protocol. Exercise training was performed on a treadmill in a progressive 10-week program. Physical training did not induce any significant changes in plasma glucose or insulin levels in diabetic rats. Total CK, CK-MM, and CK-MB activity was decreased in diabetic rat heart by 27%, 22%, and 56%, respectively. Physical training did not induce any important changes in CK activity in heart of nondiabetic rats. However, in diabetic rat heart, training increased total CK activity by 13%, CK-MM activity by 12%, and CK-MB activity by 31%. We conclude that the decrease in cardiac CK activity observed in chronic experimental diabetes mellitus can be partly alleviated by a program of physical training. This may be one of the mechanisms whereby physical conditioning improves cardiac function in experimental diabetes.
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PMID:Partial correction of impaired creatine kinase activity in diabetic rat heart by physical training. 848 78

Decreased cardiac performance is a known complication of diabetes mellitus, but the detailed molecular mechanisms that are responsible for this contractile abnormality are only incompletely explored, and cardiac gene products of known function, which are markedly and actively insulin responsive, have not been described. Recently, we found that creatine kinase (CK) enzyme activity and CK-M subunit mRNA levels are decreased in the heart of rats with experimental diabetes mellitus. These abnormalities could be restored to normal with chronic insulin administration. The CK-M and CK-B genes are expressed in the heart, and we wanted to determine whether diabetes also induces a change in CK-B mRNA levels. Quantitation of CK-M and CK-B mRNA levels on Northern blots with specific cDNA probes showed that, in diabetic hearts, CK-B mRNA levels represent only 19.8% of control levels and are more markedly depressed than CK-M mRNA levels, which are 46.5% of control values. Acute injection of insulin led to a significant 1.6-fold increase in CK-M mRNA and a 2.2-fold increase of CK-B mRNA 5 h after insulin injection. CK-M mRNA levels were restored to normal within 12 h, but 48 h were required to restore CK-B mRNA levels to normal values. After 1 mo of insulin therapy, CK-B mRNA levels had risen 9.7-fold, exceeding normal values by 90%, whereas CK-M mRNA levels were at the normal level as previously shown. CK enzyme activity showed only a small response to insulin administration 48 h postinjection. Diabetes leads therefore to a marked lowering of CK-M and CK-B mRNA levels in the rat heart.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin responsiveness of CK-M and CK-B mRNA in the diabetic rat heart. 188 84

Changes in high-energy phosphate content and cardiac contractile function of isolated rat hearts as well as changes in Ca2+ sensitivity and mitochondrial respiration of myocardial skinned fibers were assessed in hereditary cardiomyopathies and in cardiomyopathies induced by chronic treatment with adriamycin or norepinephrine, by autoimmunization, by diabetes, or by creatine deficiency. The sum of ATP and phosphocreatine contents as well as cardiac output at standard load conditions was substantially lower in almost all groups. The common features of cardiac pump failure were mild bradycardia, elevated left ventricular (LV) diastolic pressure, and stiffness that limited cardiac contractile adaptation to volume or resistance loads. The LV diastolic stiffness at maximal functional load was inversely correlated with high-energy phosphate content. Increased myofibrillar sensitivity to Ca2+ and defective function of mitochondrial creatine kinase were found in skinned myocardial fibers. These results suggested that both increased myofibrillar Ca2+ sensitivity and energy deficiency within myofibrils may contribute to increased myocardial stiffness. Increased stiffness limits LV filling but facilitates pressure development, which partly compensates for decreased contractility of cardiomyopathic hearts.
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PMID:Energy-linked functional alterations in experimental cardiomyopathies. 192 52

To assess the impact of patient age on the use of diagnostic testing in the management of acute myocardial infarction, the authors reviewed the hospital charts of 4,109 patients hospitalized for validated acute myocardial infarction in the Worcester, Massachusetts, metropolitan area during selected years between 1975 and 1986. Older patients were more likely to be female and to have a prior history of angina, hypertension, and diabetes mellitus (p less than 0.001). Acute myocardial infarctions among older patients were more likely to be recurrent, anterior in location, non-Q wave, smaller as reflected by peak creatine kinase levels, and complicated by congestive heart failure, cardiogenic shock, and atrial fibrillation (p less than 0.001). In-hospital mortality was directly related to increasing patient age (p less than 0.001). Patterns of utilization of the following diagnostic tests were examined: Holter monitoring, radionuclide ventriculography, echocardiography, exercise testing, pulmonary artery catheterization, and coronary arteriography. After adjustment for differences in demographic and clinical characteristics and in-hospital mortality, patients aged 65 years and older were significantly less likely to undergo exercise testing than were patients less than age 55. Patients older than age 75 were significantly less likely to undergo radionuclide ventriculography, pulmonary artery catheterization, and coronary arteriography than were younger patients. Sex-specific analyses did not produce results substantially different from those for the overall study population. The results of this community-wide study suggest that among patients hospitalized for acute myocardial infarction, chronologic age may be an independent determinant of utilization patterns of diagnostic testing. These findings suggest the need for a prospective evaluation of this issue, with an additional emphasis placed on the contributions of functional status and noncardiovascular illness to decision-making in the clinical management of acute myocardial infarction patients.
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PMID:Diagnostic testing in acute myocardial infarction: does patient age influence utilization patterns? The Worcester Heart Attack Study. 195 Dec 92

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

In 72 diabetic patients the serum levels of creatine kinase (CK) and its isoenzyme MB were examined together with the levels of other enzymes most frequently examined in practice. A transient elevation of the CK level, mainly of the muscular isoenzyme, was found in 12.5% of the patients examined. In none of these patients lesions of the myocardium, thyroid gland or the striated muscles, which could explain the rise of CK, were found. There was a moderate correlation between the degree of glycemia and the CK elevation but there was no such correlation with other enzymes. With improvement of the carbohydrate metabolism the CK level became normal. The possible pathogenic mechanisms for the rise of the CK level in diabetes mellitus are discussed. The limited number of the patients examined does not allow final conclusions about these mechanisms.
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PMID:[Creatine kinase in patients with diabetes mellitus]. 209 90

The urinary bladder depends on intracellular ATP for the support of a number of essential intracellular processes including contraction. The concentration of ATP is maintained constant primarily via the rapid transfer of a phosphate from creatine phosphate (CP) to ADP catalyzed by the enzyme creatine kinase (CK). Since muscular pathologies associated with diabetes are in part related to intracellular alterations in metabolism, we have characterized the CK activity in both skeletal muscle and urinary bladder from control and streptozotocin-diabetic rats. The following is a summary of the results: 1) Bladder tissue from control rats showed linear kinetics with a Vmax = 390 nmoles/mg protein/min, and a Km = 275 microM. 2) Urinary bladder tissue isolated from diabetic rats displayed biphasic kinetics with Vmax = 65 and 324 nmoles/mg protein/min, and Km's = 10 microM and 190 microM respectively. 3) Skeletal muscle isolated from control rats showed linear kinetics with an approximate Vmax of 800 nmoles/mg protein/min and a Km of 280 microM CP. 4) Homogenates of skeletal muscle from diabetic rats showed complex kinetics not separable into distinct component forms. 5) The Km for ADP for both skeletal muscle and bladder was approximately 10 microM. These studies demonstrate that whereas bladders isolated from both control and diabetic rats possess a low-affinity isomer(s) of CK with similar maximum enzymatic activity, there is a high affinity isomer present within the urinary bladder muscle of diabetic rats that is not present in bladder tissue isolated from control rats. Skeletal muscle isolated from both diabetic and control rats exhibited a maximal activity 2 to 3 times higher than that of the bladder.
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PMID:Creatine kinase activity of urinary bladder and skeletal muscle from control and streptozotocin-diabetic rats. 214 63


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