GLP-1受体激动剂对肥胖小鼠肝脏脂肪变性的影响
发布时间：2019-08-11 22:09
【摘要】：目的探讨胰高血糖素样肽1(GLP-1)受体激动剂艾塞那肽对肥胖小鼠肝脏脂肪变性及肝功能的影响。方法将8周龄雄性C57BL/6J小鼠随机分为普通饲料组(NG)和高脂饲料组(HG)喂养12周,HG组肥胖模型建模成功后再随机分为高剂量艾塞那肽组〔H组,腹腔注射0.02μg/(g·d),高脂饲料喂养〕、低剂量艾塞那肽组〔L组,腹腔注射0.01μg/(g·d),高脂饲料喂养〕、生理盐水对照组(NS组,腹腔注射等量生理盐水,高脂饲料喂养)、饮食干预组(D组,更换为普通饲料喂养)、高脂对照组(M组,继续高脂饲料喂养)进行干预,干预4周;NG组继续喂养4周。干预4周后分别测量各组小鼠的血清生化指标,包括血脂、肝功能、血糖(Glu)、尿酸(SUA)、胰岛素(INS),计算胰岛素抵抗指数(HOMA-IR),观察体质量变化情况,并取肝组织行HE染色,评估脂肪变性程度。结果治疗4周后,NS组、M组小鼠体质量均较治疗前增加(P0.001):H、L、D组小鼠体质量均较治疗前降低,且H组小鼠体质量降低较L组及D组明显(P0.05)。H组、L组、M组、NS组丙氨酸氨基转移酶(ALT)水平低于NG组(P0.05)。饮食治疗和药物治疗都可降低三酰甘油(TG)和总胆固醇(TC)至正常水平〔NS组高于NG组(P0.05),NG组与H组、L组、D组的差异无统计学意义(P0.05)〕,但H组、L组和D组在TC、TG水平的组间差异无统计学意义(P0.05)。高剂量药物治疗存在SUA水平升高的风险〔H组SUA水平高于其余各组(P0.05)〕。门冬氨酸氨基转移酶(AST)、Gly、HOMA-IR、脂肪酶(LIP)、淀粉酶(AMY)各组间差异无统计学意义(P0.05)。饮食治疗和药物治疗均可改善肝组织的脂肪变性〔NS组脂肪变性评分高于NG组(P0.05),H、L、D组脂肪变性评分与NG组差异无统计学意义(P0.05)〕。结论高剂量GLP-1受体激动剂能有效降低肥胖小鼠体质量,但在改善血脂和肝细胞脂肪变性方面与饮食干预差别不大。
[Abstract]:Objective to investigate the effect of glucagon-like peptide 1 (GLP-1) receptor agonist Essena peptide on hepatic steatosis and liver function in obese mice. Methods 8-week-old male C57BL/6J mice were randomly divided into common diet group (NG) and high-fat diet group (HG) for 12 weeks. HG group was randomly divided into high-dose eseneptide group (H group, intraabdominal injection of 0.02 渭 g / g 路d), high-fat diet) and low-dose eseneptide group (L group, intraabdominal injection of 0.01 渭 g / g 路d), high-fat diet). Saline control group (NS group, intraabdominal injection of the same amount of normal saline, high-fat feed), diet intervention group (group D, replaced by ordinary feed), high-fat control group (group M, continue high-fat feed feeding) intervention for 4 weeks; The NG group was fed for 4 weeks. After 4 weeks of intervention, serum biochemical indexes, including blood lipid, liver function, blood glucose (Glu), uric acid (SUA), insulin (INS), insulin resistance index (HOMA-IR) were calculated, the changes of body mass were observed, and the liver tissues were stained with HE to evaluate the degree of steatosis. Results after 4 weeks of treatment, the body mass of mice in NS group and M group increased compared with that before treatment (P0.001): h, L, D group decreased body mass, and H group decreased significantly compared with L group and D group (P 0.05). The level of alanine aminotransferase (ALT) in NS group was lower than that in NG group (P 0.05). Diet therapy and drug treatment could reduce (TG) and total cholesterol (TC) of triacylglycerol to normal level (NS group was higher than NG group (P 0.05), NG group, H group, L group, D group had no significant difference (P 0.05), but H group, L group and D group had no significant difference in TC,TG level (P 0.05). There was a risk of increased SUA level in high dose drug therapy (SUA level in group H was higher than that in other groups (P 0.05). There was no significant difference in aspartate aminotransferase (AST), Gly,HOMA-IR, lipase (LIP), amylase (AMY) among groups (P 0.05). Diet therapy and drug treatment could improve steatosis of liver tissue (steatosis score in NS group was higher than that in NG group (P 0.05). There was no significant difference in steatosis score between group D and NG group (P 0.05). Conclusion High dose GLP-1 receptor agonist can effectively reduce the body mass of obese mice, but it is not different from diet intervention in improving blood lipid and hepatocytic steatosis.
【作者单位】： 四川大学华西医院实验医学科;四川大学华西医院全科医学科;四川大学华西医院内分泌代谢科;
【基金】：国家自然科学基金青年项目(No.81501800和No.81400811)资助
【分类号】：R589.2
[Abstract]:Objective to investigate the effect of glucagon-like peptide 1 (GLP-1) receptor agonist Essena peptide on hepatic steatosis and liver function in obese mice. Methods 8-week-old male C57BL/6J mice were randomly divided into common diet group (NG) and high-fat diet group (HG) for 12 weeks. HG group was randomly divided into high-dose eseneptide group (H group, intraabdominal injection of 0.02 渭 g / g 路d), high-fat diet) and low-dose eseneptide group (L group, intraabdominal injection of 0.01 渭 g / g 路d), high-fat diet). Saline control group (NS group, intraabdominal injection of the same amount of normal saline, high-fat feed), diet intervention group (group D, replaced by ordinary feed), high-fat control group (group M, continue high-fat feed feeding) intervention for 4 weeks; The NG group was fed for 4 weeks. After 4 weeks of intervention, serum biochemical indexes, including blood lipid, liver function, blood glucose (Glu), uric acid (SUA), insulin (INS), insulin resistance index (HOMA-IR) were calculated, the changes of body mass were observed, and the liver tissues were stained with HE to evaluate the degree of steatosis. Results after 4 weeks of treatment, the body mass of mice in NS group and M group increased compared with that before treatment (P0.001): h, L, D group decreased body mass, and H group decreased significantly compared with L group and D group (P 0.05). The level of alanine aminotransferase (ALT) in NS group was lower than that in NG group (P 0.05). Diet therapy and drug treatment could reduce (TG) and total cholesterol (TC) of triacylglycerol to normal level (NS group was higher than NG group (P 0.05), NG group, H group, L group, D group had no significant difference (P 0.05), but H group, L group and D group had no significant difference in TC,TG level (P 0.05). There was a risk of increased SUA level in high dose drug therapy (SUA level in group H was higher than that in other groups (P 0.05). There was no significant difference in aspartate aminotransferase (AST), Gly,HOMA-IR, lipase (LIP), amylase (AMY) among groups (P 0.05). Diet therapy and drug treatment could improve steatosis of liver tissue (steatosis score in NS group was higher than that in NG group (P 0.05). There was no significant difference in steatosis score between group D and NG group (P 0.05). Conclusion High dose GLP-1 receptor agonist can effectively reduce the body mass of obese mice, but it is not different from diet intervention in improving blood lipid and hepatocytic steatosis.
【作者单位】： 四川大学华西医院实验医学科;四川大学华西医院全科医学科;四川大学华西医院内分泌代谢科;
【基金】：国家自然科学基金青年项目(No.81501800和No.81400811)资助
【分类号】：R589.2
【共引文献】
相关期刊论文 前7条
1 何，
本文编号：2525551
本文链接：https://www.wllwen.com/yixuelunwen/nfm/2525551.html
最近更新
教材专著
