Effect of long-term treatment of Carvacrol on glucose metabolism in Streptozotocin-induced diabetic mice

Yilang Li,Yunpei Mai,Xiaoxia Qiu,Wenchang Yuan,Ning Hou,Xiaoqing Chen,Conglin Li

doi:10.1186/s12906-020-02937-0

Abstract

BackgroundCarvacrol is a food additive with various bioactivities, including reducing the blood glucose level as well as improvement of heart function, in diabetic mice. We explored the antihyperglycemic effect of carvacrol and its effect on the key hepatic enzymes accounting for glucose metabolism.MethodsA streptozotocin (STZ)-induced diabetes-mellitus model in mice was used. Mice were divided randomly into a control group, diabetic group, low dose carvacrol-treated diabetic group (10 mg/kg body weight [BW]), and high dose carvacrol-treated diabetic group (20 mg/kg BW). Carvacrol was injected intraperitoneally (i.p.) in each carvacrol-treated group daily for 4 weeks and 6 weeks, respectively. The level of random plasma glucose, fasting plasma glucose, and plasma insulin was determined at 4 weeks and 6 weeks after carvacrol administration. The plasma level of total cholesterol (TC), triglycerides (TG), aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), and the activity of hepatic key enzymes related to glucose metabolism were determined.ResultsCarvacrol treatment decreased the levels of random plasma glucose and fasting plasma glucose, significantly in a dose-dependent manner. A significant improvement in glucose tolerance and a significant decrease in the plasma level of TG were observed in carvacrol-treated diabetic mice at a dose of 20 mg/kg BW compared with that in vehicle-treated diabetic mice. There was no significant difference in the plasma level of TC and insulin between vehicle-treated diabetic mice and carvacrol-treated diabetic mice. Carvacrol treatment at a dose of 20 mg/kg BW significantly reduced the plasma level of LDH but not AST, ALT, or ALP, compared with that in the vehicle-treated diabetic group. The activity of hexokinase (HK), 6-phosphofructokinase (PFK), and citrate synthetase (CS) was increased by carvacrol treatment in diabetic mice.ConclusionsCarvacrol exerted an anti-hyperglycemic effect in STZ-induced diabetic mice. This was achieved through regulating glucose metabolism by increasing the activity of the hepatic enzymes HK, PFK, and CS.

Highlights

Carvacrol is a food additive with various bioactivities, including reducing the blood glucose level as well as improvement of heart function, in diabetic mice
Carvacrol treatment for 4 weeks reduced the level of random plasma glucose to 23.52 ± 1.18 mmol/L at a dose of 10 mg/kg Body weight (BW) (T1DM + CAR10 group) and 21.07 ± 1.23 mmol/L at a dose of 20 mg/kg BW (T1DM + CAR20 group), which were significantly lower than that in the vehicle-treated diabetic group (T1DM group: 27.21 ± 0.93 mmol/L)
Carvacrol treatment at a dose of 20 mg/kg BW decreased the level of fasting plasma glucose by 21.90 and 32.70% of vehicle-treated diabetic mice at 4 weeks and 6 weeks, respectively

Summary

Introduction

Carvacrol is a food additive with various bioactivities, including reducing the blood glucose level as well as improvement of heart function, in diabetic mice. We explored the antihyperglycemic effect of carvacrol and its effect on the key hepatic enzymes accounting for glucose metabolism. An increased level of glucose in blood is associated with disturbance of carbohydrate metabolism, which is controlled by enzymes [1]. Chronic hyperglycemia and hyperlipidemia activate oxidative stress, which contributes to the development of diabetic complications, such as cardiovascular diseases, kidney injury, and retina injury [2]. Glucose homeostasis is maintained by carbohydrate-metabolism pathways such as aerobic oxidation, anaerobic glycolysis, and glycogen synthesis [3]. A set of key enzymes control carbohydrate metabolism. Citrate synthetase (CS) is a key enzyme involved in aerobic oxidation [6]. DM increases lipolysis, resulting in dyslipidemia, which accounts for the development of atherosclerosis in patients suffering from DM [8]

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