Glycyrrhizic Acid Improves Lipid and Glucose Metabolism in High-Sucrose-Fed Rats

Chanchal Chandramouli, Yong Sheau Ting, Lam Yi Lyn, Ton So Ha, Khalid Abdul Kadir


Background: The alarming increase in sugar consumption worldwide has largely contributed towards the escalating symptoms of metabolic syndrome (MetS) such as obesity, insulin resistance and dyslipidaemia. Reduction in lipoprotein lipase (LPL) activity leads to dyslipidaemia, a hallmark of MetS. Increased activation of glucocorticoid receptors also results in symptoms of MetS. Glycyrrhizic acid (GA), a triterpenoid saponin, inhibits 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1), which leads to reduced hexose-6-phosphate (H6PDH) activity and decreased glucocorticoids (GCs) production. GCs induce the gene transcriptions of enzymes such as phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase) in the gluconeogenic pathway. Studies have indicated that triterpenoids could act as PPAR agonists and GA is therefore postulated to restore LPL expression in the insulin resistant state.

Methods: Twenty-four male Sparague Dawley rats were randomly divided into three treatment groups (Group A, normal diet; Group B, high-sucrose diet; Group C, high-sucrose diet with 100 mg/kg of GA). After 28 days of treatment, the blood samples collected were analyzed for blood glucose, serum insulin and lipid profiles and the tissues collected were used for LPL expression, 11β-HSD1, H6PDH and PEPCK activities analysis. Statistical analysis was done using REST9 and SPSS softwares, P ≤ 0.05 was considered significant.

Results: Oral administration of 100mg/kg GA to high-sucrose induced rats significantly lower blood glucose (32.2%), serum insulin (68.4%), HOMA-IR (81.6%) (P < 0.05) and improved lipid parameters (P < 0.05) with no elevations in blood pressure. LPL activity was upregulated in all tissues (P > 0.05), with significant upregulation in the liver (2 fold) (P < 0.01). 11ß-HSD activity was lower in all tissues in GA treated rats compared to the group on high-sucrose diet alone (P < 0.05). Smaller elevations in H6PDH activities were observed in the liver (14.2%), kidney (7.17%), subcutaneous adipose tissue (SAT) (15.3%), abdominal muscle (AM) (18.4%) and quadriceps femoris (QF) (15.3%). PEPCK activities were elevated in the liver (14.9%) and kidney (7.0%) (P < 0.05) but increased in the SAT (74.4%) and visceral adipose tissues (VAT) (142.0%) (P < 0.01). Smaller increases were observed in the hepatic (61.6%) and renal (47.4%) G6Pase activities (P < 0.05).

Conclusion: High-sucrose feeding induced hypertension, hyperglycemia, insulin resistance and dyslipidemia. GA could ameliorate these symptoms by regulating the glucose and lipid metabolism through 11ß-HSD1 inhibition and possibly PPARγ agonism. GA induced LPL expression and contributed towards a postive shift in the lipid profiles. GA also prevented hyperglycaemia and improved insulin sensitivity in the high-sucrose fed rats without causing hypertension. Thus, GA appears to be a possible therapeutic compound in lowering the risks of developing dyslipidaemia and possibly T2DM.



Glycyrrhizic acid; Dyslipidaemia; Diabetes; Lipoprotein lipase (LPL); Phosphoenolpyruvate Carboxykinase (PEPCK); Hexose-6-Phosphate Dehydrogenase (H6PDH); Glucose-6-Phosphatase (G6Pase); 1ß-hydroxysteroid dehydrogenase 1 (11 ß-HSD)

Full Text: HTML PDF
Home     |     Log In     |      About     |      Search     |      Current     |      Archives     |      Submit      |     Subscribe



Aims and Scope

Current Issues

Conflict of Interest

About Publisher

Editorial Board



Company Profile

Editorial Office

Misconduct and Retraction


Company Registration

Contact Us

Abstracting and Indexing



Instructions to Authors


Declaration of Helsinki

Contact Publisher

Submission Checklist


Terms of Use

Company Address

Submit a Manuscript

Open Access Policy

Privacy Policy

Browse Journals

Publishing Fee

Publishing Policy


Recent Highlights

Peer-Review Process

Publishing Quality

Code of Ethics

Advertising Policy

Manuscript Tracking

Advanced Search

For Librarians


Publishing Process

Publication Frequency

For Reviewers

Propose a New Journal


Journal of Endocrinology and Metabolism, bimonthly, ISSN 1923-2861 (print), 1923-287X (online), published by Elmer Press Inc.        
The content of this site is intended for health care professionals.
This is an open-access journal distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License, which permits unrestricted
non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Creative Commons Attribution license (Attribution-NonCommercial 4.0 International CC-BY-NC 4.0)

This journal follows the International Committee of Medical Journal Editors (ICMJE) recommendations for manuscripts submitted to biomedical journals,
the Committee on Publication Ethics (COPE) guidelines, and the Principles of Transparency and Best Practice in Scholarly Publishing.

website:   editorial contact:
Address: 9225 Leslie Street, Suite 201, Richmond Hill, Ontario, L4B 3H6, Canada

© Elmer Press Inc. All Rights Reserved.