The Open Bioactive Compounds Journal


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Effects of Glycyrrhetic Acid (GE) on Some Gluconeogenic Enzymes, Lipoprotein Lipase and Peroxisome Proliferator-Activated Receptors Alpha and Gamma

Hui Ping Yaw1, *, So Ha Ton1, Khalid Abdul Kadir2, Tee Yee Tan1, Yee Wei Teo1, Michael Yohanes1
1 School of Science, Monash University Sunway Campus, Jalan Lagoon Selatan, 46150 Bandar Sunway, Selangor Darul Ehsan, Malaysia
2 School of Medicine and Health Sciences, Monash University Sunway Campus, Jalan Lagoon Selatan, 46150 Bandar Sunway, Selangor Darul Ehsan, Malaysia


The aim of this study was to examine the role of glycyrrhetic acid (GE) as a potential compound in the amelioration of metabolic syndrome. Rats given intraperitoneal injection of GE were sacrificed after 24 hours. Blood was collected for the determination of glucose, insulin and lipid profiles; while tissues were used for 11β-HSD1, gluconeogenic enzymes activities, PPAR-α/-γ and LPL expression by RT-PCR. Intraperitoneal injection of 50mg/kg GE to normal rats significantly lowered blood glucose while insulin level and HOMA-IR showed no significant changes. H6PDH activities increased in the liver, kidney, subcutaneous and visceral adipose tissues and quadriceps femoris but decreased in the abdominal muscle. PEPCK activities were significantly reduced in the kidney and decreased in the liver but showed an increase in the subcutaneous and visceral adipose tissues. G6Pase activities were found to be reduced in both the liver and kidney. 11β-HSD1 activities increased in the liver but decreased in all other tissues. There were improvements in lipid profiles in GE-treated rats. Up-regulation of LPL activity was seen in all tissues except quadriceps femoris. PPAR-α expression was up-regulated in the liver, heart and abdominal muscle while down-regulated in the kidney and quadriceps femoris but were undetectable in the subcutaneous and visceral adipose tissues. PPAR-γ expression was up-regulated in all tissues except the kidney. GE prevented hyperglycaemia and improved lipid profiles possibly through 11β-HSD1 inhibition instead of via PPAR agonism.

Keywords: : Glycyrrhetic acid, glucose-6-phosphatase (G6Pase), hexose-6-phosphate dehydrogenase (H6PDH), lipoprotein lipase, phosphoenolpyruvate kinase (PEPCK), peroxisome proliferator-activated receptors (PPAR), 11β-hydroxysteroid dehydrogenase (11β-HSD1).

Article Information

Identifiers and Pagination:

Year: 2013
Volume: 4
First Page: 14
Last Page: 24
Publisher Id: TOBCJ-4-14
DOI: 10.2174/1874847301004010014

Article History:

Received Date: 3/7/2013
Revision Received Date: 10/9/2013
Acceptance Date: 10/9/2013
Electronic publication date: 29/10/2013
Collection year: 2013

© Yaw et al.; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the 1School of Science, Monash University Sunway Campus, Jalan Lagoon Selatan, 46150 Bandar Sunway, Selangor Darul Ehsan, Malaysia; Tel: +603-55146102; Email:

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