Abstract

Glycyrrhizic acid (GA) ameliorates many components of the metabolic syndrome, but its potential therapeutic use is marred by edema caused by inhibition of renal 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2). We assessed whether 100 mg/kg per day GA administered orally could promote metabolic benefits without causing edema in rats fed on a high-sucrose diet. Groups of eight male rats were fed on one of three diets for 28 days: normal diet, a high-sucrose diet, or a high-sucrose diet supplemented with GA. Rats were then culled and renal 11β-HSD2 activity, as well as serum sodium, potassium, angiotensin II and leptin levels were determined. Histological analyses were performed to assess changes in adipocyte size in visceral and subcutaneous depots, as well as hepatic and renal tissue morphology. This dosing paradigm of GA attenuated the increases in serum leptin levels and visceral, but not subcutaneous adipocyte size caused by the high-sucrose diet. Although GA decreased renal 11β-HSD2 activity, it did not affect serum electrolyte or angiotensin II levels, indicating no onset of edema. Furthermore, there were no apparent morphological changes in the liver or kidney, indicating no toxicity. In conclusion, it is possible to reap metabolic benefits of GA without edema using the current dosage and treatment time.

Highlights

  • Metabolic syndrome is a breakdown of various metabolic functions resulting in abnormalities that pose a significant risk for cardiovascular disease and type II diabetes mellitus [1]

  • Enzyme activity was expressed in units (U), in which 1 U of 11β-HSD2 activity is defined as one picomole of 11-dehydrocorticosterone produced per 50 mg of tissue protein used, per h of incubation at 37 °C

  • Our studies have previously shown that Glycyrrhizic acid (GA) consumption attenuates the effects of a High Sucrose Diet (HSD) to increase serum glucose and insulin levels [3]

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Summary

Introduction

Metabolic syndrome is a breakdown of various metabolic functions resulting in abnormalities that pose a significant risk for cardiovascular disease and type II diabetes mellitus [1]. The characteristic aberrations of the metabolic syndrome include central obesity, hyperglycaemia, hypertension, insulin resistance and dyslipidaemia [2]. Over the past decades, decreased exercise due to improvements in technology, combined with the spread of westernized diets, have caused a significant increase in the incidence of metabolic syndrome in developed and developing countries alike [2]. Westernized diets include primarily those high in energy content, from both fat and sucrose. High-sucrose feeding alone has been shown to trigger many of the abnormalities of the metabolic syndrome [3]. The search for alternate substances that could prevent/reverse the onset and progression of the metabolic syndrome has become increasingly important

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