| With the improvement of people’s living standards,obesity shows a growing trend of morbidity.According to the World Health Organization report,obesity is growing at a remarkable rate,with approximately 1.5 billion obese and overweight people worldwide.Obesity is thought to be a chronic,low-grade inflammatory condition that causes insulin resistance and triggers a variety of diseases such as type 2 diabetes(T2DM),hyperlipidemia,hypertension and atherosclerosis.Adipose tissue is not only the organ responsible for energy storage,but also an endocrine organ that synthesizes and secretes a large number of biologically active molecules,namely adipocytokines.Among them,IL-6 and TNF-α are well-known pro-inflammatory adipocytokines.These pro-inflammatory adipocytokines are involved in the induction and maintenance of obesity-related chronic inflammatory states.When the unfolded protein accumulates too much in the endoplasmic reticulum,a stress response is induced in the endoplasmic reticulum.If the state exceeds the cell’s ability to regulate,the stress will cause cell metabolism disorder,leading to cell inflammation and apoptosis.Chitooligosaccharide refers to a water-soluble oligosaccharide composed of 2-20 monosaccharide units.Chitooligosaccharide alleviates obesity as well as insulin resistance,thus it could be applied to prevent lipid accumulation and systemic inflammation as a kind of natural edible rescources.1.In order to study the effect of high-fat diet on the obesity-induced effect of mice and the metabolism of chitooligosaccharide on obese mice induced by high-fat diet,this study used high-fat diet to build an obese mice model,body weight,fat accumulation,lipid metabolism,fasting blood glucose,serum insulin,glucose tolerance,insulin tolerance,and mouse pancreas with obese mice fed by chitooligosaccharide were prepared.Results showed that the normal diet group compared with the high-fat diet group(HF),body mass index,abdominal fat accumulation,serum total cholesterol,fasting insulin,HOMA-IR were significantly higher than the normal group.Compared with the HF group,abdominal fat accumulation,body mass index,fasting insulin,HOMA-IR were significantly lower in the chitooligosaccharide treatment group.The results suggest that a high-fat diet can successfully induce mouse fat accumulation as well as inflammation.While chitooligosaccharide can effectively alleviate the symptoms of metabolic disorders caused by high-fat diet.2.In order to study the effect of chitooligosaccharide on endoplasmic reticulum stress in adipose tissue of obese mice induced by high-fat diet.The expression of GRP-78 and PERK mRNA were detected by RT-PCR.The expression of GRP-78,PERK and NF-κB p65 protein were detected by western blotting.The results showed that the expression of GRP-78,PERK and NF-κB p65 in adipose tissue of the obese group induced by high-fat diet were higher than that of normal group.The expression of GRP-78,PERK and NF-κB p65 in adipose tissue of chitooligosaccharide intervention group were lower than that induced by high-fat diet.It is indicated that high-fat diet may induce metabolic damage in obese mice by inducing severe endoplasmic reticulum stress,and chitooligosaccharide intervention may alleviate metabolism caused by high-fat diet by reducing endoplasmic reticulum stress and inflammatory response disorders.3.Finally,this study investigated the effects of the intervention of chitosan oligosaccharide on high-fat diet-induced inflammation.Interleukin 6 and tumor necrosis factor-α from adipose tissue were detected by RT-PCR and western blotting.The results found that compared with the normal diet group,subcutaneous adipose TNF-α and IL-6 mRNA and protein expression in the high-fat diet group were significantly higher than the normal diet group,while in the chitooligosaccharide intervention group,subcutaneous adipose TNF-α and IL-6 mRNA and protein expression were significantly reduced.This suggests that the high-fat diet may cause adipose systemic inflammation and inflammatory factors releasing in obese,while chitooligosaccharide intervention is likely to prevent metabolic damage by relieving the inflammatory response. |
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