Icariin enhances AMP-activated protein kinase and prevents high fructose and high salt-induced metabolic syndrome in rats

Metabolic syndrome (MetS) is an increasing health threat and often leads to cardiovascular complications. The aim of this study was to evaluate icariin’s ability to combat MetS induced in rats and outline the involved mechanisms of action. Rats were grouped in four batches. The controls received a r...

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Main Authors: Abeer A. Aljehani, Nawal A. Albadr, Basma G. Eid, Ashraf B. Abdel-Naim
Format: Article
Language:English
Published: Elsevier 2020-11-01
Series:Saudi Pharmaceutical Journal
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S1319016420302012
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author Abeer A. Aljehani
Nawal A. Albadr
Basma G. Eid
Ashraf B. Abdel-Naim
author_facet Abeer A. Aljehani
Nawal A. Albadr
Basma G. Eid
Ashraf B. Abdel-Naim
author_sort Abeer A. Aljehani
collection DOAJ
description Metabolic syndrome (MetS) is an increasing health threat and often leads to cardiovascular complications. The aim of this study was to evaluate icariin’s ability to combat MetS induced in rats and outline the involved mechanisms of action. Rats were grouped in four batches. The controls received a regular diet and water. MetS was induced in the remaining three groups using a high-salt high-fructose diet. Groups 1 and 2 were given daily doses of saline, while Groups 3 and 4 received 25 and 50 mg/kg icariin, respectively, for 12 weeks in total. The experimental protocol was carried out for 12 weeks consecutively. Icariin significantly decreased body mass index (BMI), adiposity index and body weight. Further, icariin protected against dyslipidemia, hyperglycemia, and hyperinsulinemia and improved insulin resistance as given by the homeostatic model assessment of insulin resistance (HOMA-IR) values. Icariin guarded against the rise in serum interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α). In addition, it significantly inhibited the decrease in mRNA expression of glucose transporter type 4 (GLUT4) and liver kinase B1 (LKB1). These effects were accompanied by decreased liver content of nuclear factor kappa B (NFκB) and enhanced serum levels of phosphorylated 5ʹ-adenosine monophosphate-activated protein kinase (p-AMPK). Further, icariin significantly increased p-AMPK/AMPK ratio in liver tissues. Conclusively, icariin offers protection in experimentally induced MetS, partially due to AMPK activation.
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spelling doaj.art-86014a9337e544eb87026a7a86c476b72022-12-21T19:11:59ZengElsevierSaudi Pharmaceutical Journal1319-01642020-11-01281113091316Icariin enhances AMP-activated protein kinase and prevents high fructose and high salt-induced metabolic syndrome in ratsAbeer A. Aljehani0Nawal A. Albadr1Basma G. Eid2Ashraf B. Abdel-Naim3Department of Food Science and Nutrition, College of Food and Agriculture Sciences, King Saud University, Riyadh, Saudi ArabiaDepartment of Food Science and Nutrition, College of Food and Agriculture Sciences, King Saud University, Riyadh, Saudi ArabiaDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, King Abdulaziz University, Jeddah, Saudi ArabiaDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, King Abdulaziz University, Jeddah, Saudi Arabia; Corresponding author at: Department of Pharmacology and Toxicology, Faculty of Pharmacy, King Abdulaziz University, Jeddah, Saudi Arabia.Metabolic syndrome (MetS) is an increasing health threat and often leads to cardiovascular complications. The aim of this study was to evaluate icariin’s ability to combat MetS induced in rats and outline the involved mechanisms of action. Rats were grouped in four batches. The controls received a regular diet and water. MetS was induced in the remaining three groups using a high-salt high-fructose diet. Groups 1 and 2 were given daily doses of saline, while Groups 3 and 4 received 25 and 50 mg/kg icariin, respectively, for 12 weeks in total. The experimental protocol was carried out for 12 weeks consecutively. Icariin significantly decreased body mass index (BMI), adiposity index and body weight. Further, icariin protected against dyslipidemia, hyperglycemia, and hyperinsulinemia and improved insulin resistance as given by the homeostatic model assessment of insulin resistance (HOMA-IR) values. Icariin guarded against the rise in serum interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α). In addition, it significantly inhibited the decrease in mRNA expression of glucose transporter type 4 (GLUT4) and liver kinase B1 (LKB1). These effects were accompanied by decreased liver content of nuclear factor kappa B (NFκB) and enhanced serum levels of phosphorylated 5ʹ-adenosine monophosphate-activated protein kinase (p-AMPK). Further, icariin significantly increased p-AMPK/AMPK ratio in liver tissues. Conclusively, icariin offers protection in experimentally induced MetS, partially due to AMPK activation.http://www.sciencedirect.com/science/article/pii/S1319016420302012Metabolic syndromeIcariinAMPKNFκB
spellingShingle Abeer A. Aljehani
Nawal A. Albadr
Basma G. Eid
Ashraf B. Abdel-Naim
Icariin enhances AMP-activated protein kinase and prevents high fructose and high salt-induced metabolic syndrome in rats
Saudi Pharmaceutical Journal
Metabolic syndrome
Icariin
AMPK
NFκB
title Icariin enhances AMP-activated protein kinase and prevents high fructose and high salt-induced metabolic syndrome in rats
title_full Icariin enhances AMP-activated protein kinase and prevents high fructose and high salt-induced metabolic syndrome in rats
title_fullStr Icariin enhances AMP-activated protein kinase and prevents high fructose and high salt-induced metabolic syndrome in rats
title_full_unstemmed Icariin enhances AMP-activated protein kinase and prevents high fructose and high salt-induced metabolic syndrome in rats
title_short Icariin enhances AMP-activated protein kinase and prevents high fructose and high salt-induced metabolic syndrome in rats
title_sort icariin enhances amp activated protein kinase and prevents high fructose and high salt induced metabolic syndrome in rats
topic Metabolic syndrome
Icariin
AMPK
NFκB
url http://www.sciencedirect.com/science/article/pii/S1319016420302012
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