Abstract

The present study investigated and compared the regulatory effects on the lipid-related metabolism and intestinal disaccharidase/fecal bacterial enzyme activities between low molecular weight chitosan and chitosan oligosaccharide in high-fat-diet-fed rats. Diet supplementation of low molecular weight chitosan showed greater efficiency than chitosan oligosaccharide in suppressing the increased weights in body and in liver and adipose tissues of high-fat-diet-fed rats. Supplementation of low molecular weight chitosan also showed a greater improvement than chitosan oligosaccharide in imbalance of plasma, hepatic, and fecal lipid profiles, and intestinal disaccharidase activities in high-fat-diet-fed rats. Moreover, both low molecular weight chitosan and chitosan oligosaccharide significantly decreased the fecal microflora mucinase and β-glucuronidase activities in high-fat-diet-fed rats. These results suggest that low molecular weight chitosan exerts a greater positive improvement than chitosan oligosaccharide in lipid metabolism and intestinal disaccharidase activity in high-fat-diet-induced obese rats.

Highlights

  • Accompanying the global change in dietary consumption with western-style foods, there has been an increasing trend towards the development of metabolic syndrome-related disorders by the presence of an energy imbalance, such as obesity and diabetes mellitus (DM) [1]

  • We examined the effects of both low molecular weight chitosan (LC) and chitosan oligosaccharide (CO) on body weight, organ and tissue weights, food intake, and feed efficiency in HF-diet-fed rats

  • Previous studies are consistent with our results that supplementation of LC prevented increases in body weight and organ weight induced by feeding a HF diet in mice [18] or genetically obese mice (KK-Ay mice) [26]

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Summary

Introduction

Accompanying the global change in dietary consumption with western-style foods, there has been an increasing trend towards the development of metabolic syndrome-related disorders by the presence of an energy imbalance, such as obesity and diabetes mellitus (DM) [1]. The worldwide prevalence of obesity has more than doubled between 1980 and 2014 [2]. The global prevalence of DM among adults over 18 years of age has been elevated from 4.7% in 1980 to 8.5% in 2014 [3]. The term “diabesity” has been coined with the interdependent relationship between obesity and diabetes [4], especially type 2 DM (T2DM). Obesity and T2DM frequently occur together with the characteristics of dysregulating lipid metabolism and insulin resistance [5].

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