Abstract
This study was designed to investigate the effects of long-term feeding of chitosan on plasma glucose and lipids in rats fed a high-fructose (HF) diet (63.1%). Male Sprague-Dawley rats aged seven weeks were used as experimental animals. Rats were divided into three groups: (1) normal group (normal); (2) HF group; (3) chitosan + HF group (HF + C). The rats were fed the experimental diets and drinking water ad libitum for 21 weeks. The results showed that chitosan (average molecular weight was about 3.8 × 105 Dalton and degree of deacetylation was about 89.8%) significantly decreased body weight, paraepididymal fat mass, and retroperitoneal fat mass weight, but elevated the lipolysis rate in retroperitoneal fats of HF diet-fed rats. Supplementation of chitosan causes a decrease in plasma insulin, tumor necrosis factor (TNF)-α, Interleukin (IL)-6, and leptin, and an increase in plasma adiponectin. The HF diet increased hepatic lipids. However, intake of chitosan reduced the accumulation of hepatic lipids, including total cholesterol (TC) and triglyceride (TG) contents. In addition, chitosan elevated the excretion of fecal lipids in HF diet-fed rats. Furthermore, chitosan significantly decreased plasma TC, low-density lipoprotein cholesterol (LDL-C), very-low-density lipoprotein cholesterol (VLDL-C), the TC/high-density lipoprotein cholesterol (HDL-C) ratio, and increased the HDL-C/(LDL-C + VLDL-C) ratio, but elevated the plasma TG and free fatty acids concentrations in HF diet-fed rats. Plasma angiopoietin-like 4 (ANGPTL4) protein expression was not affected by the HF diet, but it was significantly increased in chitosan-supplemented, HF-diet-fed rats. The high-fructose diet induced an increase in plasma glucose and impaired glucose tolerance, but chitosan supplementation decreased plasma glucose and improved impairment of glucose tolerance and insulin tolerance. Taken together, these results indicate that supplementation with chitosan can improve the impairment of glucose and lipid metabolism in a HF-diet-fed rat model.
Highlights
Obesity is a worldwide health care issue and is known to increase the risk of chronic diseases, such as diabetes, hypertension, and cardiovascular disorders [1,2]
HF-diet-fed rats supplemented with chitosan had lower plasma levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) + very-low-density lipoprotein cholesterol (VLDL-C), and TC/high-density lipoprotein cholesterol (HDL-C) ratio, but the plasma TG and free fatty acid levels in HF-diet-fed rats were enhanced by the supplementation of chitosan in the diet (Table 2)
Rats fed a chitosan diet displayed decreased cholesterol and triglyceride contents in the liver (Table 4). These results indicated that chitosan feeding can reduce hepatic accumulation in rats fed a diet enriched in fructose
Summary
Obesity is a worldwide health care issue and is known to increase the risk of chronic diseases, such as diabetes, hypertension, and cardiovascular disorders [1,2]. TThhee rraattss ffeedd aann HHFF ddiieett ffoorr 2211 wweeeekkss hhaadd iinnccrreeaasseedd bbooddyy wweeiigghhtt ((FFiigguurree 11)),, lliivveerr wweeiigghhtt,, aanndd aaddiippoossee wweeiigghhtt ((TTaabbllee11)). TThhee cchhaannggeess ooff bbooddyy wweeiigghhtt iinn nnoorrmmaall aanndd ffrruuccttoosseerraattssffeeddddiiffffeerreenntt eexxppeerriimmeennttaall ddiieettss ffoorr 2211wweeeekkssiinnpprroopphhyyllaaccttiicceexxppeerriimmeenntt. The level of fasting plasma glucose in high-fructose-diet-fed rats was significantly increased, but supplementation of chitosan did not change the plasma glucose (Table 2). Dietary supplementation with chitosan significantly increased GLUT4 translocation in HF-diet-fed rat soleus muscles. Rats fed a chitosan diet displayed decreased cholesterol and triglyceride contents in the liver (Table 4) These results indicated that chitosan feeding can reduce hepatic accumulation in rats fed a diet enriched in fructose. Chitosan supplementation increased fecal cholesterol and triglyceride in rats fed a high-fructose diet (Table 5), indicating that the reduced hepatic lipid accumulation may be related to the increased fecal lipids. Normfaolr:fnnoro=rn8m=raa8ltcsroaptnsetrrpoeelra, cHehaFcgh:rohgurigopuh.pNf.ruoNrcomtromaslea:,ln:HonFromr+maClalcSoc: onhntirgtorhol,lf,HrHuFcFt:o:hsheiigg+hhcffrhruuitccottoosasseen,,;HH* FpF
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