[1]党 珊,杨 飞,吕宏军,等.GIP受体抑制剂对诱导的糖尿病小鼠糖脂代谢的研究[J].现代检验医学杂志,2017,32(05):41-43,47.[doi:10.3969/j.issn.1671-7414.2017.05.011]
 DANG Shan,YANG Fei,L(¨overU)Hong-jun,et al.Study on Glycolipid Metablism of Mice with Diabetes Induced by Peptide Receptor Antagonist Pro3(GIP)[J].Journal of Modern Laboratory Medicine,2017,32(05):41-43,47.[doi:10.3969/j.issn.1671-7414.2017.05.011]
点击复制

GIP受体抑制剂对诱导的糖尿病小鼠糖脂代谢的研究()
分享到:

《现代检验医学杂志》[ISSN:/CN:]

卷:
第32卷
期数:
2017年05期
页码:
41-43,47
栏目:
论著
出版日期:
2017-11-02

文章信息/Info

Title:
Study on Glycolipid Metablism of Mice with Diabetes Induced by Peptide Receptor Antagonist Pro3(GIP)
文章编号:
1671-7414(2017)05-041-04
作者:
党 珊1杨 飞2吕宏军2吴友伟1张 健1易 默1史丽萍1施秉银2
1.陕西省人民医院消化内二科,西安 710068; 2.西安交通大学第一附属医院内分泌科,西安 710061
Author(s):
DANG Shan1YANG Fei2L(¨overU)Hong-jun2WUYou-wei1ZHANG Jian1YI Mo1 SHI Li-ping1SHI Bing-yin2
1.the Second Department of Gastroenterology, Shaanxi Provincial People's Hospital,Xi'an 710068,China; 2.Departmentof Endocrinology, the First Affiliated Hospital of Xi'an Jiaotong University,Xi'an 710061,China
关键词:
糖依赖性胰岛素释放肽 pro3(GIP) 链脲佐菌素 糖尿病小鼠 代谢
分类号:
R-332
DOI:
10.3969/j.issn.1671-7414.2017.05.011
文献标志码:
A
摘要:
目的 研究糖依赖性胰岛素释放肽(GIP)受体抑制剂pro3(GIP)对高脂饲料和链脲佐菌素诱导的糖尿病小鼠的血糖、血脂、瘦素、脂联素以及脂肪组织炎症的影响。方法 27只小鼠随机分正常组和模型组,模型组喂食高脂饲料并注射链尿佐菌素,血糖≥16.9 mmol/L者共17只,为糖尿病模型组。将模型组分为糖尿病对照组和pro3(GIP)组,后者给予pro3(GIP)进行干预。每周追踪血糖,并进行糖耐量的测定。取小鼠血清测血脂、瘦素、脂联素,其脂肪组织进行HE染色,观察脂肪组织炎症的变化。结果 药物干预6周后,pro3(GIP)组的血糖较糖尿病组的血糖明显减低,差异有统计学显著性意义(t=8.43,P<0.01),0,30,60和120 min的胰岛素水平也均明显低于糖尿病组(t=3.90,2.60,6.88和3.33,P<0.05)。病理HE染色观察,pro3(GIP)组脂肪组织的炎症浸润较糖尿病组明显减轻,此外pro3(GIP)组血清瘦素水平显著低于糖尿病组(t=5.04,P<0.01),但两组的血清三酰甘油、胆固醇及脂联素水平均无明显差异(P>0.05)。结论 pro3(GIP)能显著地降低糖尿病小鼠的血糖、胰岛素、瘦素水平,并减轻脂肪的炎症浸润,进而调节糖尿病小鼠的代谢水平。
Abstract:
Abstract:Objective To investigate the metabolic effectsof glucose dependent insulinotropic peptide receptor antagonist pro3(GIP)in induced diabetes mice about blood glucose,triglyceride,cholesterol,leptin and fatty issue.Methods 27 C57 mice were randomly divided intonormal group and diabetes mice group,and the mice in diabetes group were fed with high fat food and intraperitoneal injected streptozocin.Then 1 mouse that random blood glucose lower than 16.9 mmol/L was deleted in diabetes group.The rest mice in diabetes group were divided into two groups,diabetes controlgroup,pro3(GIP)group.Pro3(GIP)group was given drug pro3(GIP).The bloodglucose and glucose tolerance were measured.After treatment for 6 weeks,all mice were sacrificed and fatty tissues were collected.Results After 6 weeks,the blood glucose of the pro3(GIP)group was obviously lower than diabetes control group(t=8.43,P<0.01),and insulin levers in 0,30,60 and 120 min were obviously lower than diabetes control group(t=3.90,2.60,6.88 and 3.33,P<0.05).There was significant difference between pro3(GIP)group and diabetes control group about inflammatory cells.Moreover,leptin inpro3(GIP)group was obviously lower than in diabetes control group(t=5.04,P<0.01),but triglyceride,cholesterol,and adiponectin had no significant difference between two groups.Conclusion Pro3(GIP)can significantly reduce blood glucose,insulin level,leptin of diabetes mice,and attenuate the inflammatory cells infiltration in fatty issue.

参考文献/References:

[1] Chan JC,Zhang Y,Ning G.Diabetes in China:a societal solutionfor a personal challenge[J].Lancet Diabetes Endocrinol,2014,2(12):969-979.
[2] Gault VA,O'Harte FP,Harriott P,et al.Characterization of the cellular and metabolic effects of a novel enzyme-resistant antagonist of glucose-dependent insulinotropic polypeptide[J].Biochem Biophys Res Commun,2002,290(5):1420-1426.
[3] Irwin N,McClean PL,O'Harte FP,et al.Early administration of the glucose-dependent insulinotropic polypeptide receptor antagonist pro3(GIP)prevents the development of diabetes and related metabolic abnormalities associated with genetically inherited obesity in ob/ob mice[J].Diabetologia,2007,50(7):1532-1540.
[4] Mentis N,Vardarli l,Kothe LD,et al.GIP does not potentiate the antidiabetic effects of GLP-1 in hyperglycemic patients with type 2 diabetes[J].Diabetes,2011,60(4):1270-1276.
[5] Goedecke JH,Micklesfield LK.The effect of exercise on obesity, body fat distribution and risk for type 2 diabetes[J].Med Sport Sci,2014(60):82-93.
[6] Lau E,Carvalho D,Pina-Vaz C,et al.Beyond gut microbiota:understanding obesity and type 2 diabetes[J].Hormones(Athens),2015,14(3):358-369.
[7] van Greevenbroek MM, Schalkwijk CG, Stehouwer CD.Obesity-associated low-grade inflammation in type 2 diabetes mellitus:causes and consequences[J].Neth J Med,2013,71(4):174-187.
[8] Miyawaki K,Yamada Y,Ban N,et al.Inhibition of gastric inhibitory polypeptide signaling prevents obesity[J].Nat Med,2002,8(7):738-742.
[9] Nie Y,Ma RC,Chan JC,et al.Glucose-dependent insulinotropic peptideimpairs insulin signaling via inducing adipocyte inflammation in glucose-dependent insulinotropic peptide receptor-overexpressing adipocytes[J].FASEB J,2012,26(6):2383-2393.
[10] Ranganath LR,Beety JM,Morgan LM,et al.Attenuated GLP-1 secretion in obesity:cause or consequence[J].Gut,1996,38(6):916-919.

备注/Memo

备注/Memo:
基金项目:陕西省自然科学基金项目(2014JQ4155)。 作者简介:党 珊(1980-),女,硕士,副主任医师,主要从事消化、代谢病的诊治和研究,E-mail:brightsandy@126.com。 通讯作者:施秉银,E-mail:shibingy@126.com。
更新日期/Last Update: 1900-01-01