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Hyperglycemia Induced by Glucokinase Deficiency Accelerates Atherosclerosis Development and Impairs Lesion Regression in Combined Heterozygous Glucokinase and the Apolipoprotein E-Knockout Mice
المؤلفون المشاركون
Heinonen, Suvi E.
Jönsson-Rylander, Ann-Cathrine
Adingupu, Damilola D.
Andréasson, Anne-Christine
Brusberg, Mikael
Ahnmark, Andrea
Behrendt, Margareta
Leighton, Brendan
المصدر
العدد
المجلد 2016، العدد 2016 (31 ديسمبر/كانون الأول 2016)، ص ص. 1-11، 11ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2016-09-28
دولة النشر
مصر
عدد الصفحات
11
التخصصات الرئيسية
الملخص EN
Aim.
Models combining diabetes and atherosclerosis are important in evaluating the cardiovascular (CV) effects and safety of antidiabetes drugs in the development of treatments targeting CV complications.
Our aim was to evaluate if crossing the heterozygous glucokinase knockout mouse (GK+/−) and hyperlipidemic mouse deficient in apolipoprotein E (ApoE−/−) will generate a disease model exhibiting a diabetic and macrovascular phenotype.
Methods.
The effects of defective glucokinase on the glucose metabolism and on the progression and regression of atherosclerosis on high-fat diets were studied in both genders of GK+/−ApoE−/− and ApoE−/− mice.
Coronary vascular function of the female GK+/−ApoE−/− and ApoE−/− mice was also investigated.
Results.
GK+/−ApoE−/− mice show a stable hyperglycemia which was increased on Western diet.
In oral glucose tolerance test, GK+/−ApoE−/− mice showed significant glucose intolerance and impaired glucose-stimulated insulin secretion.
Plasma lipids were comparable with ApoE−/− mice; nevertheless the GK+/−ApoE−/− mice showed slightly increased atherosclerosis development.
Conclusions.
The GK+/−ApoE−/− mice showed a stable and reproducible hyperglycemia, accelerated atherosclerotic lesion progression, and no lesion regression after lipid lowering.
This novel model provides a promising tool for drug discovery, enabling the evaluation of compound effects against both diabetic and cardiovascular endpoints simultaneously in one animal model.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Adingupu, Damilola D.& Heinonen, Suvi E.& Andréasson, Anne-Christine& Brusberg, Mikael& Ahnmark, Andrea& Behrendt, Margareta…[et al.]. 2016. Hyperglycemia Induced by Glucokinase Deficiency Accelerates Atherosclerosis Development and Impairs Lesion Regression in Combined Heterozygous Glucokinase and the Apolipoprotein E-Knockout Mice. Journal of Diabetes Research،Vol. 2016, no. 2016, pp.1-11.
https://search.emarefa.net/detail/BIM-1108290
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Adingupu, Damilola D.…[et al.]. Hyperglycemia Induced by Glucokinase Deficiency Accelerates Atherosclerosis Development and Impairs Lesion Regression in Combined Heterozygous Glucokinase and the Apolipoprotein E-Knockout Mice. Journal of Diabetes Research No. 2016 (2016), pp.1-11.
https://search.emarefa.net/detail/BIM-1108290
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Adingupu, Damilola D.& Heinonen, Suvi E.& Andréasson, Anne-Christine& Brusberg, Mikael& Ahnmark, Andrea& Behrendt, Margareta…[et al.]. Hyperglycemia Induced by Glucokinase Deficiency Accelerates Atherosclerosis Development and Impairs Lesion Regression in Combined Heterozygous Glucokinase and the Apolipoprotein E-Knockout Mice. Journal of Diabetes Research. 2016. Vol. 2016, no. 2016, pp.1-11.
https://search.emarefa.net/detail/BIM-1108290
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1108290
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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