Effects of insulin treatment on hepatic CYP1A1 and CYP2E1 activities and lipid peroxidation levels in streptozotocin-ind
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RESEARCH ARTICLE
Effects of insulin treatment on hepatic CYP1A1 and CYP2E1 activities and lipid peroxidation levels in streptozotocin-induced diabetic rats Gökçe Kuzgun 1 & Rahman Başaran 1 & Ebru Arıoğlu İnan 2 & Benay Can Eke 1 Received: 22 March 2020 / Revised: 7 August 2020 / Accepted: 17 August 2020 # Springer Nature Switzerland AG 2020
Abstract Introduction Reactive oxygen species (ROS) and lipid peroxidation (LPO) levels may increase in diabetic state and lead to oxidative stress, which plays a critical role in the progression of diabetes. There are various sources of ROS, including cytochrome P450 monooxygenases (CYP450s), which may be modulated in terms of their activities and expressions under diabetic conditions. This study is aimed to investigate the effects of streptozotocin-induced diabetes and insulin treatment on hepatic cytochrome P450 1A1 (CYP1A1) and cytochrome P450 2E1 (CYP2E1) activities and LPO levels. Methods: CYP1A1 and CYP2E1 activities were measured with ethoxyresorufin O-deethylase and p-nitrophenol hydroxylase activities, respectively. LPO levels were then corroborated via thiobarbituric acid reactive substances. Results: In diabetic rats, a marked 2.1- and 2.4-fold increase in hepatic CYP1A1 activity and 1.8- and 1.6-fold increase in hepatic CYP2E1 activity were observed compared to controls and insulin-treated diabetic rats, respectively. Hepatic LPO levels in diabetic rats did not significantly change compared to controls. However, in insulin-treated diabetic rats, LPO levels are 0.92- and 0.89-fold remarkably decrease compared to controls and diabetics, respectively. Conclusion: The present study suggests that insulin might have a useful role in the modulation of CYP1A1 and CYP2E1 activities as well as LPO levels in the liver of diabetic rats. Keywords CYP450 . CYP1A1 . CYP2E1 . Diabetes . Insulin . Streptozotocin
Introduction Diabetes mellitus is one of the most common metabolic diseases worldwide. Many studies have been carried out to clarify its mechanisms and develop more efficient therapeutic strategies. The increased oxidative stress in different tissues such as the liver, pancreas, kidney, and brain has been reported to associate with the development of diabetes and diabetic complications [1, 2]. As the liver is an essential organ in terms of its role in glucose homeostasis [3], it is crucial to understand elaborately how a diabetic state particularly affects hepatic functions.
* Benay Can Eke [email protected] 1
Present address: Department of Pharmaceutical Toxicology, Faculty of Pharmacy, Ankara University, Yenimahalle, Ankara 06560, Turkey
2
Department of Pharmacology, Faculty of Pharmacy, Ankara University, Yenimahalle, Ankara 06560, Turkey
Hyperglycaemia, or high blood glucose, is a serious symptom of diabetes. Oxidative stress can be occurred by the generation of reactive oxygen species (ROS) as a consequence of high blood glucose levels [4]. The increase in ROS production is vital due to their role in the inflammation, aging, atherosclerosis, an
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