[1]李媛 刘明明 张坚.基于新技术的糖尿病及其并发症动物模型研究进展[J].国际内分泌代谢杂志,2020,40(04):262-266.[doi:10.3760/cma.j.issn.1673-4157.2020.04.011]
　Li Yuan,Liu Mingming,Zhang Jian.Research progress in models of diabetes and diabetic complications developed from new techniques[J].International Journal of Endocrinology and Metabolism,2020,40(04):262-266.[doi:10.3760/cma.j.issn.1673-4157.2020.04.011]
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基于新技术的糖尿病及其并发症动物模型研究进展
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《国际内分泌代谢杂志》[ISSN:1673-4157/CN:12-1383/R]

卷:
40
期数:
2020年04期
页码:
262-266
栏目:
基础研究
出版日期:
2020-07-20

文章信息/Info

Title:
Research progress in models of diabetes and diabetic complications developed from new techniques
作者:
李媛 刘明明 张坚
中国医学科学院&北京协和医学院,微循环研究所,北京 100005
Author(s):
Li Yuan;  Liu Mingming;  Zhang Jian
Institute of Microcirculation, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China
关键词:
糖尿病;  动物模型;  基因编辑;  大鼠;  小鼠
Keywords:
Diabetes mellitus;  Animal models;  Gene editing;  Rat;  Mouse
DOI:
10.3760/cma.j.issn.1673-4157.2020.04.011
摘要:
因糖尿病发病机制的复杂性和受累脏器的多样性,目前尚未见可完全复现人类糖尿病疾病进程的动物模型。传统糖尿病及其并发症动物模型缺乏统一的模型建立方法和成模标准,在模型诱导和表型方面存在一定局限性。应用基因编辑和遗传育种新技术构建的糖尿病及其并发症动物模型则克服了传统诱导方法的不足,具有较好的应用价值。选择合适的糖尿病及其并发症动物模型对研究结果的可靠性和研究结论的严谨性至关重要,有助于完善糖尿病发病机制理论和新的糖尿病治疗药物筛选。
Abstract:
Due to the complexity of the pathogenesis and the diversity of the affected organs, most of traditional animal models only possess some parts of metabolic phenotypes of diabetes. Considering the lack of uniform inducing protocol and modeling standards, there are shortcomings in the induction and phenotype among traditional models of diabetes and diabetic complications. Application of gene editing and genetic breeding to generate the models of diabetes and diabetic complications conquer some of the shortcomings mentioned above, which contains considerable application value. Therefore, it is crucial to choose appropriate animal models to ensure the reliability of research data and the conclusion. Furthermore, it may be helpful for understanding the pathogenesis of diabetes and contributing to the development of anti-diabetic drugs.

参考文献/References:

[1] Sheen JM,Hsieh CS,Tain YL,et al.Programming effects of prenatal glucocorticoid exposure with a postnatal high-fat diet in diabetes mellitus[J].Int J Mol Sci,2016,17(4):533. DOI:10.3390/ijms17040533.
[2] Lang J,Wang X,Liu K,et al.Oral delivery of staphylococcal nuclease by Lactococcus lactis prevents type 1 diabetes mellitusin NOD mice[J].Appl Microbiol Biotechnol,2017,101(20):7653-7662. DOI:10.1007/s00253-017-8480-5.
[3] Eizirik DL,Op de Beeck A.Coxsackievirus and type 1 diabetes mellitus: The Wolf's Footprints[J].Trends Endocrinol Metab,2018,29(3):137-139.DOI:10.1016/j.tem.2017.12.002.
[4] 邢玮,王政霖,吕甜甜,等.2型糖尿病db/db小鼠的生物学特性[J].中国比较医学杂志,2017,27(8):12-15.DOI:10.3969.j.issn.1671-7856.2017.08.003.
[5] Guest PC.Characterization of the Goto-Kakizaki(GK)rat model of type 2 diabetes[J].Methods Mol Biol,2019,1916:203-211.DOI:10.1007/978-1-4939-8994-2_19.
[6] Han F,Li X,Yang J,et al.Salsalate prevents β-cell dedifferentiation in OLETF rats with type 2 diabetes through notch1 pathway[J].Aging Dis,2019,10(4):719-730.DOI:10.14336/AD.2018.1221.
[7] Du J,Dong W,Li H,et al.Protective effects of IFN-γ on the kidney of type- 2 diabetic KKAy mice[J].Pharmacol Rep,2018,70(3):607-613.DOI:10.1016/j.pharep.2017.12.009.
[8] Ogura Y,Kitada M,Monno I,et al.Renal mitochondrial oxidative stress is enhanced by the reduction of Sirt3 activity, in Zuckerdiabetic fatty rats[J].Redox Rep,2018,23(1):153-159.DOI:10.1080/13510002.2018.1487174.
[9] Lee VK,Hosking BM,Holeniewska J,et al.BTBR ob/ob mouse model of type 2 diabetes exhibits early loss of retinal function and retinal inflammation followed by late vascular changes[J].Diabetologia,2018,61(11):2422-2432.DOI:10.1007/s00125-018-4696-x.
[10] Mosa R,Huang L,Wu Y,et al.Hexarelin, a growth hormone secretagogue, improves lipid metabolic aberrations in nonobese insulin-resistant male MKR mice[J].Endocrinology,2017,158(10):3174-3187.DOI:10.1210/en.2017-00168.
[11] Pouwer MG,Heinonen SE,Behrendt M,et al.The APOE 3-leiden heterozygous glucokinase knockout mouse as novel translational disease model for type 2 diabetes, dyslipidemia, and diabetic atherosclerosis[J].J Diabetes Res,2019,2019:9727952. DOI:10.1155/2019/9727952.
[12] Katsuda Y,Kemmochi Y,Maki M,et al.Effects of unilateral nephrectomy on renal function in male Spontaneously Diabetic Torii fattyrats:a novel obese type 2 diabetic model[J].J Diabetes Res,2014,2014:363126.DOI:10.1155/2014/363126.
[13] 张玉倩,刘笑迎,贾岩辉,等. 糖尿病性脑内微小病变大鼠模型的建立及其病理学研究[J].国际内分泌代谢杂志,2019,39(2):83-86.DOI:10.3760/cma.j.issn.1673-4157.2019.02.003.
[14] Maekawa T,Ohta T,Kume S.Pathophysiological abnormalities in the brains of spontaneously diabetic torii-lepr fa(SDT fatty)rats, a novel type 2 diabetic model[J].J Vet Med Sci,2018,80(9):1385-1391.DOI:10.1292/jvms.18-0296.
[15] Ou Y,Ren Z,Wang J,et al.Phycocyanin ameliorates alloxan-induced diabetes mellitus in mice: involved in insulin signalingpathway and GK expression[J].Chem Biol Interact,2016,247:49-54.DOI:10.1016/j.cbi.2016.01.018.
[16] Gonçalves DA,Silveira WA,Manfredi LH,et al.Insulin/IGF1 signalling mediates the effects of β2-adrenergic agonist on muscle proteostasis and growth[J].J Cachexia Sarcopenia Muscle,2019,10(2):455-475.DOI:10.1002/jcsm.12395.
[17] Parilla JH,Willard JR,Barrow BM,et al.A mouse model of beta-cell dysfunction as seen in human type 2 diabetes[J].J Diabetes Res,2018,2018:6106051.DOI:10.1155/2018/6106051.
[18] Wang-Fischer Y,Garyantes T.Improving the reliability and utility of streptozotocin-induced rat diabetic model[J].J Diabetes Res,2018,2018:8054073. DOI:10.1155/2018/8054073.
[19] Adachi SI,Yoshizawa F,Yagasaki K.Hyperuricemia in type 2 diabetic model KK-Ay/Ta mice: a potent animal model with positivecorrelation between insulin resistance and plasma high uric acid levels[J].BMC Res Notes,2017,10(1):577.DOI:10.1186/s13104-017-2897-x.
[20] Nakano K,Yanobu-Takanashi R,Takahashi Y,et al.Novel murine model of congenital diabetes: the insulin hyposecretion mouse[J].J Diabetes Investig,2019,10(2):227-237. DOI:10.1111/jdi.12895.
[21] Sakimura K,Maekawa T,Sasagawa K,et al.Depression-related behavioural and neuroendocrine changes in the Spontaneously Diabetic Torii(SDT)fatty rat, an animal model of type 2 diabetes mellitus[J].Clin Exp Pharmacol Physiol,2018,[Epub ahead of print].DOI:10.1111/1440-1681.12965.
[22] Maekawa T, Tadaki H, Sasase T,et al. Pathophysiological profiles of SDT fatty rats, a potential new diabetic peripheral neuropathy model[J].J Pharmacol Toxicol Methods,2017,88(Pt 2):160-166.DOI:10.1016/j.vascn.2017.09.257.
[23] Luce S,Guinoiseau S,Gadault A,et al.Humanized mouse model to study type 1 diabetes[J].Diabetes,2018,67(9):1816-1829.DOI:10.2337/db18-0202.
[24] Bornfeldt KE,Kramer F,Batorsky A,et al.A novel type 2 diabetes mouse model of combined diabetic kidney disease and atherosclerosis[J].Am J Pathol,2018,188(2):343-352.DOI:10.1016/j.ajpath.2017.10.012.
[25] Hunter CA,Kartal F,Koc ZC,et al.Mitochondrial oxidative phosphorylation is impaired in TALLYHO mice, a new obesity and type 2 diabetes animal model[J].Int J Biochem Cell Biol,2019,116:105616.DOI:10.1016/j.biocel.2019.105616.
[26] Sun G,Jackson CV,Zimmerman K,et al.The FATZO mouse, a next generation model of type 2 diabetes, develops NAFLD and NASH when fed a western diet supplemented with fructose[J].BMC Gastroenterol,2019,19(1):41.1-11.DOI:10.1186/s12876-019-0958-4.
[27] Liao Z,Zhang J,Wang J,et al.The anti-nephritic activity of a polysaccharide from okra(abelmoschus esculentus(L.)moench)via modulation of AMPK-Sirt1-PGC-1α signaling axis mediated anti-oxidative in type 2 diabetesmodel mice[J].Int J Biol Macromol,2019,140:568-576.DOI:10.1016/j.ijbiomac.2019.08.149.
[28] Fan J,Campioli E,Papadopoulos V.Nr5a1-Cre-mediated tspo conditional knockout mice with low growth rate and prediabetessymptoms-A mouse model of stress diabetes[J].Biochim Biophys Acta Mol Basis Dis,2019,1865(1):56-62.DOI:10.1016/j.bbadis.2018.10.022.

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备注/Memo

备注/Memo:
通信作者:刘明明,Email: mingmingliu@imc.pumc.edu.cn
基金项目:国家自然科学基金(81900747)
Corresponding author: Liu Mingming, Email:mingmingliu@imc.pumc.edu.cn
Fund program:National Natural Science Foundation of China(81900747)
更新日期/Last Update: 2020-07-20