Pleiotropic ameliorative effects of ellagitannin geraniin against metabolic syndrome induced by high-fat diet in rats.

Objectives: Metabolic syndrome (MetS), a multiplex risk factor for cardiovascular disease and type 2 diabetes, is increasingly prevalent worldwide. Ellagitannin geraniin, a polyphenol found in the rind of rambutan (Nephelium lappaceum), has demonstrated therapeutic effects against metabolism dysfunction. The aim of this study was to characterize the metabolic effects and possible mechanism of geraniin in rats with MetS induced by a high-fat diet (HFD).

The insulin-sensitising properties of the ellagitannin geraniin and its metabolites from rind in 3T3-L1 cells.

In this study, the insulin-like and insulin sensitising effects of the ellagitannins geraniin, corilagin, ellagic acid, gallic acid and rind extract in 3T3-L1 adipocytes was investigated. It was observed that non-toxic concentrations of geraniin and its metabolites (0.2-20 μM) and extract (0.

Purified ingredient-based high-fat diet is superior to chow-based equivalent in the induction of metabolic syndrome.

The present study aimed to outline the physiological and metabolic disparity between chow- and purified ingredient-based high-fat diets and their efficacy in the induction of metabolic syndrome (MetS). Male, 3-week-old Sprague Dawley rats were randomly assigned to chow-based control diet, chow-based high-fat diet, purified control diet, and purified high-fat diet for 12 weeks. Physical and biochemical changes were documented.

Increased susceptibility of post-weaning rats on high-fat diet to metabolic syndrome.

The present study aimed to examine the effects of the types of high-calorie diets (high-fat and high-fat-high-sucrose diets) and two different developmental stages (post-weaning and young adult) on the induction of metabolic syndrome. Male, post-weaning and adult (3- and 8-week old, respectively) Sprague Dawley rats were given control, high-fat (60% kcal), and high-fat-high-sucrose (60% kcal fat + 30% sucrose water) diets for eight weeks (n = 6 to 7 per group). Physical, biochemical, and transcriptional changes as well as liver histology were noted.

The Ameliorative Effects of a Tocotrienol-Rich Fraction on the AGE-RAGE Axis and Hypertension in High-Fat-Diet-Fed Rats with Metabolic Syndrome.

The clinical value of tocotrienols is increasingly appreciated because of the unique therapeutic effects that are not shared by tocopherols. However, their effect on metabolic syndrome is not well-established. This study aimed to investigate the effects of a tocotrienol-rich fraction (TRF) from palm oil in high-fat-diet-treated rats.

Glycyrrhizic acid prevents high calorie diet-induced metabolic aberrations despite the suppression of peroxisome proliferator-activated receptor γ expression.

Objective: To investigate the effects of glycyrrhizic acid supplementation on glucose and lipid metabolism in rodents consuming a high-fat, high-sucrose diet.

Methods: Twenty-four male, 8-week old Sprague Dawley rats with an initial weight of 160 to 200 g were randomised into three groups (n = 6 for each group): groups A (standard rat chow), B (high-fat, high-sucrose diet), and C (high-fat, high-sucrose diet + 100 mg/kg/d of glycyrrhizic acid via oral administration). The rats were treated accordingly for 4 wk.

Modulation of lipid metabolism in glycyrrhizic acid-treated rats fed on a high-calorie diet and exposed to short or long-term stress.

Stress and high-calorie diets increase the risk of developing metabolic syndrome. Glycyrrhizic acid (GA) has been shown to improve dyslipidaemia in rats fed on a high-calorie diet. This study aimed to examine the effects of GA on lipid metabolism in rats exposed to short- or long-term stress and on a high-calorie diet.

Glycyrrhizic acid can attenuate metabolic deviations caused by a high-sucrose diet without causing water retention in male Sprague-Dawley rats.

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.

Novel Inhibitory Effects of Glycyrrhizic Acid on the Accumulation of Advanced Glycation End Product and Its Receptor Expression.

Beneficial effects of glycyrrhizic acid (GA), a bioactive extract of licorice root, in the prevention of metabolic syndrome have been consistently reported while advanced glycation end products (AGE) and receptor for advanced glycation end product (RAGE) are the leading factors in the development of diabetes mellitus. The aim of this study was to investigate the effects of GA on the AGE-RAGE axis using high-fat/high-sucrose (HF/HS) diet-induced metabolic syndrome rat models. Twenty four male Sprague-Dawley rats were randomly assigned into three groups for 4 weeks: (1) Group A, normal diet with standard rat chow; (2) Group B, HF/HS diet; (3) Group C, HF/HS diet and oral administration of 100 mg/kg GA per day.

Irregularities in glucose metabolism induced by stress and high-calorie diet can be attenuated by glycyrrhizic acid.

Stress and high-calorie diet increase the risk of developing metabolic syndrome. Glycyrrhizic acid (GA) has been shown to improve hyperglycaemia and dyslipidaemia under various physiological conditions. This study was aimed at examining the effects of stress and GA on glucose metabolism under short- or long-term stress.

Stress and Its Effects on Glucose Metabolism and 11β-HSD Activities in Rats Fed on a Combination of High-Fat and High-Sucrose Diet with Glycyrrhizic Acid.

Chronic stress has been shown to have a strong link towards metabolic syndrome (MetS). Glycyrrhizic acid (GA) meanwhile has been shown to improve MetS symptoms caused by an unhealthy diet by inhibiting 11 β -HSD 1. This experiment aimed to determine the effects of continuous, moderate-intensity stress on rats with and without GA intake on systolic blood pressure (SBP) across a 28-day period, as well as glucose metabolism, and 11 β -HSD 1 and 2 activities at the end of the 28-day period.

Amelioration of glucose homeostasis by glycyrrhizic acid through gluconeogenesis rate-limiting enzymes.

The activities of phosphoenolpyruvate carboxykinase (PEPCK) are influenced by active glucocorticoids which are activated by 11-β-hydroxysteroid dehydrogenase 1 (11β-HSD1) while hexose-6-phosphate dehydrogenase (H6PDH) influences the activities of 11-βHSD1 in a cofactor manner. Dysregulation of PEPCK and H6PDH has been associated with the pathogenesis of metabolic syndrome. Sixteen male Sprague Dawley rats, fed ad libitum, were assigned to two groups, control and treated, with the treated group being given GA at 100mg/kg for one week.

Glycyrrhizic acid improved lipoprotein lipase expression, insulin sensitivity, serum lipid and lipid deposition in high-fat diet-induced obese rats.

Background: The metabolic syndrome, known also as the insulin resistance syndrome, refers to the clustering of several risk factors for atherosclerotic cardiovascular disease. Dyslipidaemia is a hallmark of the syndrome and is associated with a whole body reduction in the activity of lipoprotein lipase (LPL), an enzyme under the regulation of the class of nuclear receptors known as peroxisome proliferator-activated receptor (PPAR). Glycyrrhizic acid (GA), a triterpenoid saponin, is the primary bioactive constituent of the roots of the shrub Glycyrrhiza glabra.

Effects of Glycyrrhizic Acid on Peroxisome Proliferator-Activated Receptor Gamma (PPARgamma), Lipoprotein Lipase (LPL), Serum Lipid and HOMA-IR in Rats.

Studies on ligand binding potential of glycyrrhizic acid, a potential agonist to PPARgamma, displayed encouraging results in amelioration of metabolic syndrome. The regulation of gene cassettes by PPARgamma affects glucose homeostasis, lipid, lipoprotein metabolism and adipogenesis. This study was performed to determine the effects of GA on total PPARgamma and LPL expression levels, lipid parameters and HOMA-IR.

Lipoprotein lipase expression, serum lipid and tissue lipid deposition in orally-administered glycyrrhizic acid-treated rats.

Background: The metabolic syndrome (MetS) is a cluster of metabolic abnormalities comprising visceral obesity, dyslipidaemia and insulin resistance (IR). With the onset of IR, the expression of lipoprotein lipase (LPL), a key regulator of lipoprotein metabolism, is reduced. Increased activation of glucocorticoid receptors results in MetS symptoms and is thus speculated to have a role in the pathophysiology of the MetS.