高脂肪饮食小鼠体重增加和代谢变化

J. L. Pereira, Priscilla Cristovam Sampaio e Souza, Vivian Izumi Shinzato, Sandramara Sasso, Bruna Larissa Spontoni do Espirito Santo, Lidiani Figueiredo Santana, Tamy Ingrid Restel, K. Freitas
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引用次数: 1

摘要

目的:探讨高脂饮食对C57BL/6小鼠肥胖及糖脂代谢紊乱的诱导作用。材料与方法:将动物分为两组,共19只C57BL/6小鼠:对照组(商品饲粮;N =9)和试验组(高脂饮食;n = 10)。12周内测定各组的进食量和增重,计算食物效率系数(FEC)和致氧指数(Aterogenic Index)。进行口服糖耐量试验(TOTG),绘制血糖曲线,测定曲线下面积(AUC)。解剖肝脏和脂肪组织(AT)部位,对肝脏和附睾脂肪组织进行组织学分析。计算肥胖指数(AI%),测定总胆固醇、总胆固醇组分、葡萄糖、血清甘油三酯浓度。结果:试验组大鼠进食量显著降低(p<0.001),总增重显著提高(p=0.001), FEC显著提高(p<0.001)。实验组大鼠附睾(p<0.001)、腹膜后(p<0.001)、肠系膜(p=0.002)、肾周AT (p=0.012)、总脂肪(p<0.001)、AI% (p<0.001)升高。实验组总胆固醇较高(p=0.025),对照组HDL较低(p=0.005)。实验组脂肪细胞面积也高于对照组(p=0.049)。其他参数组间差异无统计学意义。结论:该模型在短时间内诱导肥胖,并以低成本饮食促进内脏脂肪增加。进一步的研究需要提高其效率,并完全改变C57BL/6小鼠的血脂和血糖。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Ganho de peso e alterações metabólicas em camundongos submetidos à dieta hiperlipídica
Objective: The aim of this study was to evaluate the efficiency of high fat diet in the induction of obesity and glucose and lipid metabolism disorders in C57BL/6 mice. Materials and Methods: Animals were organized into two groups, totalizing 19 C57BL/6 mice: control group (commercial diet; n=9) and experimental group (high fat diet; n=10). Food intake and weight gain were measured during 12 weeks and Food Efficiency Coefficient (FEC) and Aterogenic Index were calculated. The Oral Glucose Tolerance Test (TOTG) was performed, the glycemic curve was constructed and the area under the curve (AUC) was verified. Liver and adipose tissue (AT) sites were dissected and histological analysis of the liver and epididymal adipose tissue were performed. The Adiposity Index (AI%) was calculated and the concentration of total cholesterol, its fractions, glucose and serum triglycerides were measured. Results: The experimental group presented lower food intake (p<0.001) and higher total weight gain (p=0.001) and FEC (p<0.001). It was observed in the experimental group an increase in the epididymal (p<0.001), retroperitoneal (p<0.001), mesenteric (p=0.002), perirenal AT (p=0.012), total fat (p <0.001) and AI% (p<0.001). Total cholesterol was higher in the experimental group (p=0.025) and the HDL lower in the control group (p=0.005). The adipocyte area of the experimental group was also higher than the control group (p=0.049). In the other parameters there was no significant difference between groups. Conclusion: This model induced obesity in a short period of time and promoted increased visceral adiposity with a low-cost diet. Further studies are needed to improve its efficiency and to completely change blood lipids and glycemia in C57BL/6 mice.
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