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The APOE∗3-Leiden Heterozygous Glucokinase Knockout Mouse as Novel Translational Disease Model for Type 2 Diabetes, Dyslipidemia, and Diabetic Atherosclerosis
المؤلفون المشاركون
Jukema, Jan Wouter
Pieterman, Elsbet J.
Heinonen, Suvi E.
Jönsson-Rylander, Ann-Cathrine
Andréasson, Anne-Christine
Behrendt, Margareta
Leighton, Brendan
Pouwer, Marianne G.
van Koppen, Arianne
Menke, Aswin L.
Princen, Hans M. G.
van den Hoek, Anita M.
المصدر
العدد
المجلد 2019، العدد 2019 (31 ديسمبر/كانون الأول 2019)، ص ص. 1-13، 13ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2019-02-21
دولة النشر
مصر
عدد الصفحات
13
التخصصات الرئيسية
الملخص EN
Background.
There is a lack of predictive preclinical animal models combining atherosclerosis and type 2 diabetes.
APOE∗3-Leiden (E3L) mice are a well-established model for diet-induced hyperlipidemia and atherosclerosis, and glucokinase+/− (GK+/−) mice are a translatable disease model for glucose control in type 2 diabetes.
The respective mice respond similarly to lipid-lowering and antidiabetic drugs as humans.
The objective of this study was to evaluate/characterize the APOE∗3-Leiden.glucokinase+/− (E3L.GK+/−) mouse as a novel disease model to study the metabolic syndrome and diabetic complications.
Methods.
Female E3L.GK+/−, E3L, and GK+/− mice were fed fat- and cholesterol-containing diets for 37 weeks, and plasma parameters were measured throughout.
Development of diabetic macro- and microvascular complications was evaluated.
Results.
Cholesterol and triglyceride levels were significantly elevated in E3L and E3L.GK+/− mice compared to GK+/− mice, whereas fasting glucose was significantly increased in E3L.GK+/− and GK+/− mice compared to E3L.
Atherosclerotic lesion size was increased 2.2-fold in E3L.GK+/− mice as compared to E3L (p=0.037), which was predicted by glucose exposure (R2=0.636, p=0.001).
E3L and E3L.GK+/− mice developed NASH with severe inflammation and fibrosis which, however, was not altered by introduction of the defective GK phenotype, whereas mild kidney pathology with tubular vacuolization was present in all three phenotypes.
Conclusions.
We conclude that the E3L.GK+/− mouse is a promising novel diet-inducible disease model for investigation of the etiology and evaluation of drug treatment on diabetic atherosclerosis.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Pouwer, Marianne G.& Heinonen, Suvi E.& Behrendt, Margareta& Andréasson, Anne-Christine& van Koppen, Arianne& Menke, Aswin L.…[et al.]. 2019. The APOE∗3-Leiden Heterozygous Glucokinase Knockout Mouse as Novel Translational Disease Model for Type 2 Diabetes, Dyslipidemia, and Diabetic Atherosclerosis. Journal of Diabetes Research،Vol. 2019, no. 2019, pp.1-13.
https://search.emarefa.net/detail/BIM-1173482
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Pouwer, Marianne G.…[et al.]. The APOE∗3-Leiden Heterozygous Glucokinase Knockout Mouse as Novel Translational Disease Model for Type 2 Diabetes, Dyslipidemia, and Diabetic Atherosclerosis. Journal of Diabetes Research No. 2019 (2019), pp.1-13.
https://search.emarefa.net/detail/BIM-1173482
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Pouwer, Marianne G.& Heinonen, Suvi E.& Behrendt, Margareta& Andréasson, Anne-Christine& van Koppen, Arianne& Menke, Aswin L.…[et al.]. The APOE∗3-Leiden Heterozygous Glucokinase Knockout Mouse as Novel Translational Disease Model for Type 2 Diabetes, Dyslipidemia, and Diabetic Atherosclerosis. Journal of Diabetes Research. 2019. Vol. 2019, no. 2019, pp.1-13.
https://search.emarefa.net/detail/BIM-1173482
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1173482
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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