Elevated levels of serum glucose, triglyceride, and liver enzymes in a rat model of 7,12 dimethylbenz[a]anthracene (DMBA)-induced carcinogenesis
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ABSTRACT Background: Uncontrolled cell proliferation in cancers has a high requirement of energy and biosynthetic substrates. Glucose and triglycerides are the main source of energy as well as the primary building blocks for forming cellular components of mammalian cells.Objective: This study aims to evaluate the shifting of serum glucose, triglyceride, and nitrogen wastes in the form of urea and creatinine levels; and liver enzymes levels, alanine transaminase (ALT) and aspartate aminotransferase (AST), in rat model carcinogenesis with a single dose of 7,12-dimethylbenzanthracene (DMBA) for 16 weeks observation..Methods: The experimental animals of Rattus norvegicus strain Sprague Dawley were divided into two groups, namely the control group and the DMBA-induced group. A blood chemistry examination was carried out at weeks 4, 8, 12, and 16 post-induction using a spectrophotometer. In addition, observation of breast tumor formation and histological examination of the tumor and organs, including liver, lung, intestine, and kidney, were performed to confirm cancer formation.Results: Five of the six experimental rats (83.3%) induced by DMBA experienced breast and lung cancer formation accompanied by continuous weight loss starting at week 10 after induction. Serum glucose levels increased significantly at weeks 12 and 16 after induction, while serum triglyceride, ALT, and AST levels increased significantly from week 4 after induction until the end of the experiment. Serum urea levels did not show a significant difference from the control group. Nonetheless, creatinine decreased at the last examination.Conclusion: Elevated serum glucose, triglycerides, ALT, and AST levels escorted the chemical carcinogen-induced cancer development. Studies at the clinical level are needed to prove whether abnormally elevated of these blood chemistry levels can be used to detect the presence of cancer early.Keywords:DMBA, breast cancer, lung cancer, cancer metabolism.Keywords:
Blood urea nitrogen
Aspartate transaminase
7,12-Dimethylbenz[a]anthracene
Transaminase
AIM:To evaluate the hepatic dysfunction in leptospirosis is usually mild and resolved eventually.However, sequential follow-up of liver biochemical data remained lacking.. METHODS:The biochemistry data and clinical symptoms of 11 sporadic patients were collected and analyzed, focusing on the impacts of leptospirosis upon liver biochemistry tests. RESULTS:The results disclosed that of the 11 cases, 5 or 45% died.The liver biochemistry data in the beginning of the disease course were only mildly elevated.Nevertheless, late exaggerated aspartate transaminase (AST) elevations were noted in three cases who finally died when compared with the typical course.Besides, significant higher AST/alanine transaminase (ALT) ratios (AARs) of the peak levels for transaminase were also noted in the cases who eventually succumbed.The mean±SD of AARs for the survival group and dead group were 5.65±2.27(n = 5) and 1.86±0.64(n = 6) respectively (P = 0.006).The ratios of the cases who finally died were all more than 3.0.Conversely, the survival group's ratios were less than 3.0. CONCLUSION:Serial follow-up of transaminase might provide evidence to predict some rare evolutions in leptospirosis.If AST elevated progressively without a concomitant change of ALT, it might indicate an acute disease course with ensuing death.Additionally, AAR is another prognostic parameter for leptospirosis.Once the value was higher than 3.0, a grave prognosis is inevitable.
Aspartate transaminase
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Elevated transaminases
Alanine aminotransferase
Liver disease
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Drug-induced liver injury was most common in clinical therapy.The levels of alanine transaminase(ALT)and aspartate transaminase(AST)in 1242 in-patient children and 953 healthy chidren were analyzed in this paper.A significantly high levels of AST and ALT activity (more than 40IU/L)were observed in in-patient children,being 26.08% and 31.00% as com- pared to that of 3.99% and 3.16% in healthy children,respectively,showing significant difference.
Aspartate transaminase
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Alanine aminotransferase
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Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels are widely used as sensitive markers of possible tissue damage, particularly liver toxicity. Lipid-lowering drugs, such as fibrates, slightly increase serum transaminase levels in humans, but there is little evidence that the phenomenon is related to drug-induced liver injury (DILI). Some in vitro studies have indicated that the elevations of serum transaminase activities after treatment of humans with fenofibrate, one of the fibrates, are related to increased transaminase synthesis in the hepatocytes rather than to transaminase leakage from the hepatocytes associated with cell lysis. In this study, male F344/DuCrlCrlj (Fischer) rats were treated once with fenofibrate at a dose level of 400 mg/kg and the relationships between the pharmacological effects, blood and hepatic transaminase activities and the gene expression of the transaminases in the liver were investigated. Fenofibrate treatment slightly increased plasma transaminase activities in rats with the findings directly related to the pharmacological action of the drug. The increases were in parallel with increases in hepatic transaminase activities associated with increases in the transaminase genes in the liver and were not considered to be a consequence of hepatotoxicity from the drug. The modification in transaminase gene expression is likely to be secondary to the pharmacological action of fenofibrate. The evidence obtained in our study underlines the importance of gene regulation as a possible alternative mechanism for increased blood transaminase activities.
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Fenofibrate
Aspartate transaminase
Steatosis
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Summary Alanine transaminase activity in the liver of adult rats (350–450 gm.) fell progressively from the 10th through the 30th day of growth of Walker carcinoma 256. The enzyme activity decreased to a level about 30 per cent of that found in comparable rats of the same age without tumors. Loss of enzyme activity occurred concurrently, with a gradual loss of carcass weight. Treatment with cortisol (4 mg/kg, administered during the first 10 days of tumor growth) increased the activity of alanine transaminase in liver 2.5-fold, but the same dose did not alter transaminase activity when the tumors were large (days 20 through 30). The activity of this transaminase could be raised to normal in the presence of large tumors by feeding a diet containing 75 per cent casein. When this high-protein diet was fed, treatment with cortisol (4 mg/kg) increased alanine transaminase activity fourfold. Tyrosine transaminase and tryptophan pyrrolase differed from alanine transaminase in that both of these enzymes were increased four- to fivefold by cortisol (10 mg/kg) in the livers of rats with established Walker tumors.
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Aspartate transaminase level was significantly increased in intestine of experimentals that received multiple doses of infection. The level of alanine transaminase rose to a significant value in liver of mice infected with multiple doses. Rise of transaminases is correlated with the necrosis (disruption of intestina) hepatic cells in infected mice. Changes and/or the distribution of aspartate transaminase and alanine transaminase with regard to the dosage is discussed.
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Transaminase
Ancylostoma caninum
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Aspartate transaminase
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AIM: To evaluate the hepatic dysfunction in leptospirosis is usually mild and resolved eventually. However,sequential follow-up of liver biochemical data remained lacking..METHODS: The biochemistry data and clinical symptoms of 11 sporadic patients were collected and analyzed, focusing on the impacts of leptospirosis upon liver biochemistry tests.RESULTS: The results disclosed that of the 11 cases, 5 or 45% died. The liver biochemistry data in the beginning of the disease course were only mildly elevated.Nevertheless, late exaggerated aspartate transaminase (AST)elevations were noted in three cases who finally died when compared with the typical course. Besides, significant higher AST/alanine transaminase (ALT) ratios (AARs) of the peak levels for transaminase were also noted in the cases who eventually succumbed. The mean±SD of AARs for the survival group and dead group were 5.65±2.27 (n = 5)and 1.86±0.64 (n = 6) respectively (P= 0.006). The ratios of the cases who finally died were all more than 3.0.Conversely, the survival group's ratios were less than 3.0.CONCLUSION: Serial follow-up of transaminase might provide evidence to predict some rare evolutions in leptospirosis. If AST elevated progressively without a concomitant change of ALT, it might indicate an acute disease course with ensuing death. Additionally, AAR is another prognostic parameter for leptospirosis. Once the value was higher than 3.0, a grave prognosis is inevitable.
Aspartate transaminase
Transaminase
Elevated transaminases
Concomitant
Alanine aminotransferase
Liver disease
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A little is known about the prevalence of elevated alanine transaminase in a Moroccan healthy population. Our aim was to search for the upper limit of normal alanine transaminase in the blood donors and then to apply the upper limit of normal alanine found in the population so as to assess the prevalence of subjects with abnormal transaminase level. We then, investigated for factors associated with increased level of transaminase in our population. This study was carried out on 14071 blood donors, (74.1% of men and 25.9% female) aged between 18 to 60 years, randomly chosen. Serum transaminase activity was measured using on IEMS Reader, Labsystems. Hepatitis B and C were performed by ELISA. The upper limit of normal transaminase found were 64 for men and 52 for women. Consequently, 2.08% blood donors had an abnormal level of transaminase. Follow up results revealed that drug was the first cause of elevated transaminase in our cohort followed by diet and alcohol consumption. One seroconversion for hepatitis C was identified. In conclusion, this study showed that even though there is an evident lack of efficiency in using alanine aminotransferase testing qualifying blood donors in our country, preventing viral potential transmission through transfusions was possible.
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Alanine aminotransferase
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Objective To investigate the relationship between transaminase anomaly and prognosis. in severe brain injury. Methods Total 117 cases with severe traumatic brain injury from January 2010 to June 2012 were admitted and detect the blood level of the alanine transarninase (ALT) and glutamic-oxal(o)acetic transaminase (AST). Transaminase anomaly included ALT 50 U/L and (or) AST 50 U/L. According to the test results, they were divided into transaminase anomaly group and normal group. The level of ALT, AST and different GOS prognostic score were compared in both groups. Results The favorable prognosis rate in transaminase anomaly group was lower than that of the normal group (χ2=4.71, P0.05), with the mortality higher than that of normal group (χ2=5.42, P0.05). The level of ALT and AST in transaminase anomaly group was significantly related with GOS prognosis, and the higher transaminase level is, the worse the prognosis. Conclusion Transaminase elevated level are often contributed to severe traumatic brain injury. The careful monitoring and protection of the liver function have a favorable effect on improvement of the prognosis of brain injury patients.
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Elevated transaminases
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Eighty-six patients who required heparin therapy were randomly assigned to receive bovine or porcine heparin. Abnormal concentrations of alanine transaminase and aspartate transaminase developed during treatment in 59.3% and 26.7% of patients, respectively. Patient characteristics that significantly influenced the development of abnormal alanine transaminase concentrations were male sex and higher baseline enzyme values. Transaminase concentrations returned to normal in 80% of patients after heparin therapy was discontinued and in 20% during therapy. Analysis of transaminase concentrations in all 86 patients showed that 95% had some increase in enzymes during treatment. Mean maximal increase over baseline for all patients was 3.6 for alanine transaminase and 3.1 for aspartate transaminase (range, 1.0 to 15). Lactate dehydrogenase concentrations became abnormal in 35.7% of patients. Lactate dehydrogenase isoenzyme determinations in 6 patients showed elevated hepatic fractions. No clinical symptoms of hepatic dysfunction were seen.
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