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

The present study investigated the possible protective effects of Casearia esculenta root extract on certain biochemical markers in streptozotocin (STZ)-induced diabetes in rats. STZ treatment (50 mg/kg, ip) caused a hyperglycemic state, that led to various physiological and biochemical alterations. Blood levels of glucose, urea, uric acid and creatinine, plasma levels of albumin and albumin/globulin ratio and the activities of diagnostic marker enzymes aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and gamma-glutamyltranspeptidase (gamma-GT) in plasma, liver and kidney were markedly altered in STZ diabetic rats. Oral administration of C. esculenta (200 and 300 mg/kg) for 45 days restored all these biochemical parameters to near normal levels. Thus, the present results have shown that C. esculenta root extract has the antihyperglycemic effect and consequently may alleviate liver and renal damage associated with STZ-induced diabetes in rats.
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PMID:Influence of Casearia esculenta root extract on protein metabolism and marker enzymes in streptozotocin-induced diabetic rats. 1559 47

Insulin resistance (IR), glucose intolerance and diabetes mellitus are commonly associated with cirrhosis. The exact pathogenetic mechanisms responsible are still unknown; however, they may be related to both hepatitis C virus itself and to liver injury. IR may be the earliest abnormality, which in the following years may progress to clinical diabetes mellitus. The aim of this study was to investigate the presence of IR by euglycaemic hyperinsulinemic clamp technique, in chronic hepatitis C patients. 15 patients and nine healthy controls without any known condition that may affect IR were enrolled to the study. Chronic hepatitis C was diagnosed by liver biopsy (hepatic activity index was also determined in 10 patients) and appropriate viral and biochemical tests. Eight patients were given interferon therapy, which had been stopped for at least 3 months before the study. Euglycaemic hyperinsulinemic clamp technique was performed as previously described and peripheral glucose utilisation rate, M value, was calculated in mg/kg/min by infusion of 40 IU/m2/min regular insulin. M value of the control group was significantly higher than that of chronic hepatitis C patients (M = 5.1+/-1 vs. 3.7+/-1; p = 0.004), which was consistent with IR in the patient group. There was no significant correlation between the M value and alanine aminotransferase, aspartate aminotransferase and hepatic activity index (p = 0.621, 0.549, 0.479, respectively). Our results suggest that IR is present in chronic hepatitis C patients; it is not directly related to hepatic injury, moreover, it may be associated with some component(s) inherent to hepatitis C virus.
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PMID:Insulin resistance in chronic hepatitis C. 1560 64

Mild elevations in liver chemistry tests such as alanine transaminase and aspartate transaminase can reveal serious underlying conditions or have transient and benign etiologies. Potential causes of liver transaminase elevations include viral hepatitis, alcohol use, medication use, steatosis or steatohepatitis, and cirrhosis. The history should be thorough, with special attention given to the use of medications, vitamins, herbs, drugs, and alcohol; family history; and any history of blood-product transfusions. Other common health conditions, such as diabetes, heart disease, and thyroid disease, can cause or augment liver transaminase elevations. The recent American Gastroenterological Association guideline regarding the evaluation and management of abnormal liver chemistry tests proposes a practical, algorithmic approach when the history and physical examination do not reveal the cause. In addition to liver chemistries, an initial serologic evaluation includes a prothrombin time; albumin; complete blood count with platelets; hepatitis A, B, and C serologies; and iron studies. Depending on the etiology, management strategies may include cessation of alcohol use, attention to medications, control of diabetes, and modification of lifestyle factors such as obesity. If elevations persist after an appropriate period of observation, further testing may include ultrasonography and other serum studies. In some cases, biopsy may be indicated.
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PMID:Mildly elevated liver transaminase levels in the asymptomatic patient. 1579 89

Metformin is a biguanide derivate used as an oral hypoglycaemic drug in diabetics. The aim of this study was to examine the histological and biochemical effects of metformin in streptozotocin (STZ)-treated rats. The animals were rendered diabetic by intraperitoneal injection of 65 mg/kg STZ. Fourteen days later, metformin was given at 25 mg/kg by gavage, daily for 28 days, to STZ-diabetic rats and a control group. In the STZ-diabetic group, some degenerative changes were observed by light microscopic examination. But the degenerative changes were decreased in the STZ-diabetic group given metformin. In the STZ-diabetic group, blood glucose levels, serum alanine and aspartate transaminase (ALT and AST) activities, total lipid levels, and sodium and potassium levels increased, while body weight, serum magnesium levels and liver glutathione (GSH) levels decreased. In the STZ-diabetic group given metformin, blood glucose levels, serum ALT and AST activities, total lipid, and sodium and potassium levels decreased, and liver GSH and serum magnesium levels increased. As a result of all the morphological and biochemical findings obtained, it was concluded that metformin has a protective effect against the hepatotoxicity produced by STZ diabetes.
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PMID:Protective effects of metformin treatment on the liver injury of streptozotocin-diabetic rats. 1590 Oct 52

Non-enzymatic glycation as the chain reaction between reducing sugars and free amino groups of proteins has been shown to correlate with physiological ageing and severity of diabetes. The process involves oxidative steps (glycoxidation). In this paper, the effect of D-fructose as a reactive sugar on aspartate aminotransferase (AST) as a model protein was monitored by measurements of the enzyme activity and formation of fluorescent advanced glycation end products (AGEs). Change in the AST activity was considered as a measure of the overall protein damage caused by glycation, and total AGEs and pentosidine represent, at least partly, the formation of glycoxidation products. Catalytic activity of AST in an incubation mixture containing D-fructose (50 mmol L(-1)), decreased compared to control values to 42% (p < 0.05) and to 11% (p < 0.05) on the 5th and on 21st day of incubation, respectively. In the presence of fructose, total fluorescent AGEs concentration was significantly higher since 5th day of incubation (110%, p < 0.05) and the fluorescent pentosidine concentration from 15th day of incubation (117%, p < 0.05) compared to control values, respectively. Catalytic activity of AST clearly and quantitatively demonstrated functional changes in the enzyme molecule caused by structural modifications initiated by fructose, while the evaluation of AGE formation and especially that of pentosidine by fluorescence measurement was less reliable.
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PMID:Enzyme activity and AGE formation in a model of AST glycoxidation by D-fructose in vitro. 1590 28

Hyperglycemia increases the generation of free radicals by glucose auto-oxidation, and the increment of free radicals may lead to liver cell damage. In this study, we tested the hypothesis that hyperglycemia-induced increases of serum liver enzymes among its physiological concentration would be inversely associated with serum antioxidant carotenoid level. Study subjects were 857 male and female Japanese who had received health examinations in 2003. Those with a history of liver disease and excessive alcohol drinkers were excluded. The associations of serum six-carotenoid concentrations with serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) stratified by glucose tolerance status were evaluated cross-sectionally. Serum AST and ALT concentrations in the groups of impaired fasting glucose (IFG) and diabetes were significantly higher than those in the normal group. The multivariate-adjusted means of the serum AST and ALT concentrations in IFG and diabetes group were significantly low in accordance with the tertiles of the serum beta-cryptoxanthin and beta-carotene concentrations. The most inverse association of serum liver enzyme and carotenoid concentration was observed in beta-cryptoxanthin. Antioxidant carotenoid, especially beta-cryptoxanthin, may act a deterrent substance against increasing the serum aminotransferase in the earlier pathogenesis of liver dysfunction among hyperglycemic subjects.
Diabetes Res Clin Pract 2006 Jan
PMID:Serum carotenoid concentrations are inversely associated with serum aminotransferases in hyperglycemic subjects. 1600 96

Previously, we reported high hepatotoxic sensitivity of type 2 diabetic (DB) rats to three dissimilar hepatotoxicants. Additional work revealed that a normally nonlethal dose of CCl4 was lethal in DB rats due to inhibited compensatory tissue repair. The present study was conducted to investigate the importance of compensatory tissue repair in determining the final outcome of hepatotoxicity in diabetes, using another structurally and mechanistically dissimilar hepatotoxicant, thioacetamide (TA), to initiate liver injury. A normally nonlethal dose of TA (300 mg/kg, ip), caused 100% mortality in DB rats. Time course studies (0 to 96 h) showed that in the non-DB rats, liver injury initiated by TA as assessed by plasma alanine or aspartate aminotransferase and hepatic necrosis progressed up to 48 h and regressed to normal at 96 h resulting in 100% survival. In the DB rats, liver injury rapidly progressed resulting in progressively deteriorating liver due to rapidly expanding injury, hepatic failure, and 100% mortality between 24 and 48 h post-TA treatment. Covalent binding of 14C-TA-derived radiolabel to liver tissue did not differ from that observed in the non-DB rats, indicating similar bioactivation-based initiation of hepatotoxicity. S-phase DNA synthesis measured by [3H]-thymidine incorporation, and advancement of cells through the cell division cycle measured by PCNA immunohistochemistry, were substantially inhibited in the DB rats compared to the non-DB rats challenged with TA. Thus, inhibited cell division and compromised tissue repair in the DB rats resulted in progressive expansion of liver injury culminating in mortality. In conclusion, it appears that similar to type 1 diabetes, type 2 diabetes also increases sensitivity to dissimilar hepatotoxicants due to inhibited compensatory tissue repair, suggesting that sensitivity to hepatotoxicity in diabetes occurs in the absence as well as presence of insulin.
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PMID:Type 2 diabetic rats are sensitive to thioacetamide hepatotoxicity. 1615 71

Glycation is common posttranslational modification of proteins impairing their function, which occurs during diabetes mellitus and aging. Beside extracellular glycation of long-lived proteins, intracellular modifications of short-lived proteins by more reactive sugars like fructose are possible. The process includes free oxygen radicals (glycoxidation). In an attempt to reduce glycoxidation and formation of advanced glycation products (AGE), influence of 0.2-1.2 mM uric acid as endogenous antioxidant on glycoxidation of purified pig heart aspartate aminotransferase (AST) by 50 mM and 500 mM D-fructose in vitro was studied. Uric acid at 1.2 mM concentration reduced AST activity decrease and formation of total AGE products caused by incubation in vitro of the enzyme with sugar up to 25 days at 37 degrees C. The results thus support the hypothesis that uric acid has beneficial effects in controlling protein glycoxidation. The in vitro system AST-fructose proved to be a useful tool for investigation of glycation process.
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PMID:Glycation-induced inactivation of aspartate aminotransferase, effect of uric acid. 1618 93

Nonalcoholic fatty liver disease (NAFLD) is emerging as a component of the metabolic syndrome, although it is not known whether markers of NAFLD, including elevated concentrations of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALK), predict the development of metabolic syndrome. Our objective was to investigate the associations of elevated AST, ALT, and other liver markers, including C-reactive protein (CRP), with incident National Cholesterol Education Program-defined metabolic syndrome among 633 subjects in the Insulin Resistance Atherosclerosis Study who were free of metabolic syndrome at baseline. Insulin sensitivity (Si) and acute insulin response (AIR) were directly measured from the frequently sampled intravenous glucose tolerance test among African-American, Hispanic, and non-Hispanic white subjects aged 40-69 years. After 5.2 years, 127 individuals had developed metabolic syndrome. In separate logistic regression models adjusting for age, sex, ethnicity, clinic, and alcohol consumption, subjects in the upper quartiles of ALT, ALK, and CRP were at significantly increased risk of incident metabolic syndrome compared with those in the lowest quartile: ALT, odds ratio 2.50 (95% CI 1.38-4.51); ALK, 2.28 (1.24-4.20); and CRP, 1.33 (1.09-1.63). Subjects in the upper quartile of the AST-to-ALT ratio were at significantly reduced metabolic syndrome risk (0.40 [0.22-0.74]). After further adjustment for waist circumference, Si, AIR, and impaired glucose tolerance, the associations of ALT and the AST-to-ALT ratio with incident metabolic syndrome remained significant (ALT, 2.12 [1.10-4.09]; the AST-to-ALT ratio, 0.48 [0.25-0.95]). These associations were not modified by ethnicity or sex, and they remained significant after exclusion of former and heavy drinkers. In conclusion, NAFLD markers ALT and the AST-to-ALT ratio predict metabolic syndrome independently of potential confounding variables, including directly measured Si and AIR.
Diabetes 2005 Nov
PMID:Liver markers and development of the metabolic syndrome: the insulin resistance atherosclerosis study. 1624 37

Strychnos potatorum Linn. seeds are used in the Indian traditional system of medicine for the treatment of hepatopathy, nephropathy, gonorrhoea, leucorrhoea, gastropathy, bronchitis, chronic diarrhoea, strangury, renal and vesicle calculi, diabetes and eye diseases. The present study describes the hepatoprotective and antioxidant activities of the seed powder (SPP) and aqueous extract (SPE) of Strychnos potatorum seeds against CCl4-induced acute hepatic injury. Hepatic injury was achieved by injecting 3 ml/kg, s.c. of CCl4 in equal proportion with olive oil. Both SPP and SPE at the doses 100 and 200 mg/kg, p.o. offered significant (p < 0.001) hepatoprotective action by reducing the serum marker enzymes like serum glutamate oxaloacetate transaminase (SGOT) and serum glutamate pyruvate transaminase (SGPT). They also reduced the elevated levels of ALP and serum bilirubin. Reduced enzymic and nonenzymic antioxidant levels and elevated lipid peroxide levels were restored to normal by administration of SPP and SPE. Histopathological studies further confirmed the hepatoprotective activity of SPP and SPE when compared with the CCl4 treated control groups. The results obtained were compared with Silymarin (50 mg/kg, p.o.), the standard drug. In conclusion, SPE (200 mg/kg, p.o.) showed significant hepatoprotective activity similar to that of the standard drug, Silymarin (50 mg/kg, p.o.).
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PMID:Studies on hepatoprotective and antioxidant actions of Strychnos potatorum Linn. seeds on CCl4-induced acute hepatic injury in experimental rats. 1638 23


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