Effect of polycan, a β-glucan originating from Aureobasidium, on a high-fat diet-induced hyperlipemic hamster model

Abstract

The aim of the present study was to analyze the effect of polycan, a β-glucan originating from Aureobasidium, on high-fat diet (HFD)-induced hyperlipemia and hepatic damage. A total of 30 hamsters were divided into 6 groups based on their body weight following acclimatization: control, sham, simvastatin (SIMVA) and 3 Polycan groups. In the polycan groups, Polycan, at three concentrations (31.25, 62.5 and 125 mg/kg), was administered orally once a day for 56 days, in addition to the HFD. On the day of sacrifice, changes in the body weight, food consumption, liver weight and serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglyceride and total cholesterol (T-CHOL) were observed, as well as changes to the liver and aorta (thoracic and abdominal) histopathology and histomorphometry. The results from the polycan groups were compared with a SIMVA 10 mg/kg oral treatment group, in addition to the sham and vehicle control groups. After the HFD-induced hyperlipidemic hamsters were administered Polycan, there was no significant change in their body weight and food consumption when compared with the hamsters in the vehicle control group. However, the serum levels of AST, ALT, triglyceride, T-CHOL and LDL were significantly reduced in a dose-dependent manner when compared with the vehicle control group (P<0.05). Furthermore, the levels of liver steatosis and arteriosclerosis in the abdominal and thoracic aorta were significantly decreased in a dose-dependent manner (P<0.01). In the SIMVA-treated group, body weight (P<0.05), the serum level of lipids (triglyceride, T-CHOL and LDL; P<0.01) and the level of arteriosclerosis (P<0.01) were significantly reduced when compared with the vehicle control group. However, liver weight and the serum levels of AST, ALT, and liver steatosis increased when compared with the vehicle control group. Based on these results, it was concluded that polycan exerts a favorable effect in decreasing HFD-induced hyperlipemia and associated atherosclerosis, with relatively good protective effects on liver damage.

Oral administration of Pantoea agglomerans-derived lipopolysaccharide prevents development of atherosclerosis in high-fat diet-fed apoE-deficient mice via ameliorating hyperlipidemia, pro-inflammatory mediators and oxidative responses

“…These findings suggested that the lowering effect of plasma ox-LDL levels by orally administered LPSp may be mediated partly via the reduction of oxidative burst responses. Oral administration of β-glucan, which is considered as an immunostimulant and non-absorbable polysaccharide, was shown to decrease HFD-fed induced oxidative stress and development of atherosclerotic plaques in a rodent model [ 40 ]. These beneficial effects may be results of improvement of microbiota profiles and intestinal immune system [ 41 ].…”

Effects of Glucan and Vitamin D Supplementation on Obesity and Lipid Metabolism in Diabetic Retinopathy

“…Dietary fiber fractions from mushrooms were found to modulate cholesterol-related gene expression [ 33 ]. Lim [ 34 ] used a hamster experimental model to apply β-glucans (“polycan”) from yeast-like fungus Aureobasidium pullulans . The authors concluded that polycan decreased the atherosclerotic effects, hyperlipemia, and hepatic damage of liver, which were induced by means of high-fat diet.…”

β-glucans and cholesterol (Review)

“…These hamsters have a number of advantages: As in humans, their primary cholesterol carrier in the plasma is LDL, their lipoprotein metabolism is similar to that of humans 84 and their LDL receptor gene is similar to the LDL gene in humans. Lim et al ( 127 ) applied β-glucans from yeast-like fungus Aureobasidium pullulans , known as polycan, to a hamster experimental animal model of hyperlipemia induced by a high-fat diet. The authors concluded that polycan decreased the atherosclerotic effects, hyperlipemia and hepatic damage induced by a high-fat diet.…”