| Objective To establish the obese rats model induced by high fat diet. To evaluate theeffects of cyanidin-3-glucoside (C3G) on body weight, visceral adipose tissue, lipidprofiles, inflammatory cytokines, and insulin resistance in high-fat diet-induced obeserats. Then, to analyze the relationship between body weight, visceral adipose tissue,lipid profiles, inflammatory cytokines and insulin resistance. Finally, to explore themechanism of cyanidin-3-glucoside regulates body weight, lipid profiles, inflamma-tory cytokines, and insulin resistance in high-fat diet-induced obese rats.Methods Thirty male Sprague-Dawley rats were randomly grouped to receive a stan-dard chow diet (n=8) or high fat diet (n=22). Five weeks later,17high-fat di-et-induced obese rats were randomly divided into two groups. Then, rats were re-ceived a standard chow diet supplemented with normal saline (control group), ahigh-fat diet supplemented with normal saline (obese group), or a high-fat diet sup-plemented with cyanidin-3-glucoside (C3G group) at100mg/(kg·d) for5weeks andwere then euthanized. Parameters of body weight, visceral adipose tissue and foodintake were measured. Blood samples were collected for detecting total cholesterol,triglyceride, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol,tumor necrosis factor-α, interleukin-6, monocyte chemoattractant protein-1, fastingglucose, fasting insulin. Then, Insulin resistance index and average feed efficiencyratio (FER) were calculated. Finally, the data was analyzed by SPSS19.0software.Results At the end of the research, the level of body weight [(434.0±20.7)g], visceraladipose tissue[(4.73±0.14)g/100g body weight], energy intake[(415±24)KJ/d], FER [(1.44±0.05)%], TC[(61.6±7.1)mg/dL], TG [(17.8±2.4)mg/dL], LDL-C[(27.4±5.8)mg/dL], TNF-α[(7.6±1.9)ng/L], IL-6[(4.6±0.8)ng/L], MCP-1[(4.6±1.0) ng/L],FPG[(11.3±1.5)mmol/L], FINS[(11.9±1.2)mIU/mL], and IRI(5.6±1.0) in obesegroup were higher than those in control group [They were(351.7±20.7)g,(3.25±0.20)g/100g body weight,(299±19)KJ/d,(1.31±0.05)%,(45.3±3.9)mg/dL,(12.0±2.3)mg/dL,(16.3±4.6)mg/dL,(3.7±1.0)ng/L,(1.7±0.5)ng/L,(2.7±0.6)ng/L,(7.4±2.5)mmol/L,(7.3±2.0)mIU/mL,2.4±0.6, respectively], and the differences were signifi-cant(all P<0.05). The level of HDL-C[(27.4±5.8) mg/dL] in obese group was higherthan that in control group[(16.3±4.6) mg/dL], and the difference was significant(P<0.05). The level of body weight [(408.7±17.4) g], visceral adipose tissue[(4.17±0.12)g/100g body weight],energy intake [(420±24) KJ/d], FER[(1.08±0.08)%],TC[(54.8±2.0)mg/dL], TG[(14.7±2.6)mg/dL), LDL-C[(22.1±2.7)mg/dL), TNF-α[(4.6±1.2)ng/L], IL-6[(2.4±0.6)ng/L], MCP-1[(3.6±1.0)ng/L], FPG [(9.2±1.3)mmol/L], FINS[(9.1±1.7)mmol/L], and IRI(3.8±1.0) in C3G group were lower than those inobese group, but the levels of the paremeters in C3G group were significantly higherthan those in the control group (P<0.05). The level of HDL-C [(22.1±2.7)mg/dL] inC3G group were significantly higher than that in the obese group (P<0.05). Other pa-rameters showed no significant changes. The level of insulin resistance index was po-sitively correlated with body weight, visceral adipose tissue, TC, TG, LDL-C, TNF-α,IL-6, MCP-1, FPG, FINS, and the correalation coefficients were0.733,0.668,0.602,0.607,0.683,0.728,0.784,0.907and0.743(all P<0.01). The insulin resistance indexwas negatively correalated with HDL-C, and the correalation coefficient is-0.581(P<0.01).Conclusions Obesity causes metabolic dysfunction of glucose and lipid, low gradeinflammation, and insulin resistance. Dietary supplementation with cyaniding-3-glucoside suppresses body weight gain and visceral adipose tissue by enhancingenergy expenditure, and alleviates insulin resistance in high-fat diet-induced obeserats via attenuating dylipidemia,and low grade inflammation. |
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