The Effect of Insulin induced Hypoglycemia on ketoconazole Hepatototxicity in Rabbit

Background: Hypoglycemia is one of the most common side effect of insulin treatment, it affect liver and can potentiate ketoconazole toxicity. Objectives: To measure effect of ketoconazole on liver enzymes, hypoglycemic oxidative stress and to evaluate if N-acetylcysteine, can modulate this effec...

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Main Authors: Nabeel A.J.Ali, Riyad H. Zayer Anaed
Format: Article
Language:English
Published: University of Basrah 2015-06-01
Series:The Medical Journal of Basrah University
Subjects:
Online Access:https://mjbu.uobasrah.edu.iq/article_103870_511adeba58e5118ffa2fa5030df68561.pdf
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author Nabeel A.J.Ali
Riyad H. Zayer Anaed
author_facet Nabeel A.J.Ali
Riyad H. Zayer Anaed
author_sort Nabeel A.J.Ali
collection DOAJ
description Background: Hypoglycemia is one of the most common side effect of insulin treatment, it affect liver and can potentiate ketoconazole toxicity. Objectives: To measure effect of ketoconazole on liver enzymes, hypoglycemic oxidative stress and to evaluate if N-acetylcysteine, can modulate this effect. Methods: Thirty five male rabbits were randomly divided into five groups: Group 1: (control group), Group 2:( ketoconazole), Group 3: (insulin), Group 4: ( ketoconazole+ insulin), Groups 5: (ketoconazole + insulin + N-Acetyl cysteine). Animals were sacrificed at day 3. Blood collected for measurement of liver enzymes, and total bilirubin. Malondialdehyde and glutathione were measured in serum and liver. Results: Ketoconazole increased serum and liver malondialdehyde, 0.594 ± 0.17 and 4614.49 ± 1288.00 nmol/gm. Increased aspartate aminotransferase 38.19 ± 17.29 and alkaline phosphatase 29.29 ± 10.2 U/L. Insulin increased serum malondialdehyde 0.522 ± 0.19, alkaline phosphatase 15.77 ± 6.12 U/L and bilirubin 0.56 ± 0.26 mg/dl. Ketoconazole + insulin, increased serum malondialdehyde 0.850 ± 0.16 µmol/l and bilirubin 0.77 ± 0.55 mg/dl. Ketoconazole + insulin increased serum malondialdehyde 0.850 ± 0.16 µmol/l, aspartate amino transferase 54.35 ± 18.34 U/L, alanine amino transferase, 34.74 ± 11.08 U/L, alkaline pohospahtase 30.81 ± 12.4 U/L and bilirubin 2.51 ± 1.55 mg/dl. N-acetylcysteine reduced aspartate aminotransferase 28.12 ± 22.21 U/L, alkaline phosphatase 11.81 ± 3.03 IU/L) and bilirubin 0.39 ± 0.18 mg/dl Conclusion: Hypoglycemia caused hepatotoxicity and oxidative stress and potentiates the toxicity of ketoconazole. N-acetylcysteine partly reverse this hepatotoxicity.
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spelling doaj.art-db2be86c70ac4b4fb2fd7f4c82de88a12022-12-22T03:11:28ZengUniversity of BasrahThe Medical Journal of Basrah University0253-07592413-44142015-06-01331172310.33762/mjbu.2015.103870103870The Effect of Insulin induced Hypoglycemia on ketoconazole Hepatototxicity in RabbitNabeel A.J.AliRiyad H. Zayer AnaedBackground: Hypoglycemia is one of the most common side effect of insulin treatment, it affect liver and can potentiate ketoconazole toxicity. Objectives: To measure effect of ketoconazole on liver enzymes, hypoglycemic oxidative stress and to evaluate if N-acetylcysteine, can modulate this effect. Methods: Thirty five male rabbits were randomly divided into five groups: Group 1: (control group), Group 2:( ketoconazole), Group 3: (insulin), Group 4: ( ketoconazole+ insulin), Groups 5: (ketoconazole + insulin + N-Acetyl cysteine). Animals were sacrificed at day 3. Blood collected for measurement of liver enzymes, and total bilirubin. Malondialdehyde and glutathione were measured in serum and liver. Results: Ketoconazole increased serum and liver malondialdehyde, 0.594 ± 0.17 and 4614.49 ± 1288.00 nmol/gm. Increased aspartate aminotransferase 38.19 ± 17.29 and alkaline phosphatase 29.29 ± 10.2 U/L. Insulin increased serum malondialdehyde 0.522 ± 0.19, alkaline phosphatase 15.77 ± 6.12 U/L and bilirubin 0.56 ± 0.26 mg/dl. Ketoconazole + insulin, increased serum malondialdehyde 0.850 ± 0.16 µmol/l and bilirubin 0.77 ± 0.55 mg/dl. Ketoconazole + insulin increased serum malondialdehyde 0.850 ± 0.16 µmol/l, aspartate amino transferase 54.35 ± 18.34 U/L, alanine amino transferase, 34.74 ± 11.08 U/L, alkaline pohospahtase 30.81 ± 12.4 U/L and bilirubin 2.51 ± 1.55 mg/dl. N-acetylcysteine reduced aspartate aminotransferase 28.12 ± 22.21 U/L, alkaline phosphatase 11.81 ± 3.03 IU/L) and bilirubin 0.39 ± 0.18 mg/dl Conclusion: Hypoglycemia caused hepatotoxicity and oxidative stress and potentiates the toxicity of ketoconazole. N-acetylcysteine partly reverse this hepatotoxicity.https://mjbu.uobasrah.edu.iq/article_103870_511adeba58e5118ffa2fa5030df68561.pdfinsulinsitagliptintype
spellingShingle Nabeel A.J.Ali
Riyad H. Zayer Anaed
The Effect of Insulin induced Hypoglycemia on ketoconazole Hepatototxicity in Rabbit
The Medical Journal of Basrah University
insulin
sitagliptin
type
title The Effect of Insulin induced Hypoglycemia on ketoconazole Hepatototxicity in Rabbit
title_full The Effect of Insulin induced Hypoglycemia on ketoconazole Hepatototxicity in Rabbit
title_fullStr The Effect of Insulin induced Hypoglycemia on ketoconazole Hepatototxicity in Rabbit
title_full_unstemmed The Effect of Insulin induced Hypoglycemia on ketoconazole Hepatototxicity in Rabbit
title_short The Effect of Insulin induced Hypoglycemia on ketoconazole Hepatototxicity in Rabbit
title_sort effect of insulin induced hypoglycemia on ketoconazole hepatototxicity in rabbit
topic insulin
sitagliptin
type
url https://mjbu.uobasrah.edu.iq/article_103870_511adeba58e5118ffa2fa5030df68561.pdf
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