Development of NASH in Obese Mice is Confounded by Adipose Tissue Increase in Inflammatory NOV and Oxidative Stress
المؤلفون المشاركون
Sacerdoti, David
Abraham, Nader G.
Rezzani, Rita
Singh, Shailendra P.
Raffaele, Marco
Lebovics, Edward
Schragenheim, Joseph
Vanella, Luca
Meissner, Aliza
Grant, Ilana
Rodella, Luigi F.
Bamshad, David
Favero, Gaia
Bellner, Lars
المصدر
International Journal of Hepatology
العدد
المجلد 2018، العدد 2018 (31 ديسمبر/كانون الأول 2018)، ص ص. 1-14، 14ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2018-07-02
دولة النشر
مصر
عدد الصفحات
14
التخصصات الرئيسية
الملخص EN
Aim.
Nonalcoholic steatohepatitis (NASH) is the consequence of insulin resistance, fatty acid accumulation, oxidative stress, and lipotoxicity.
We hypothesize that an increase in the inflammatory adipokine NOV decreases antioxidant Heme Oxygenase 1 (HO-1) levels in adipose and hepatic tissue, resulting in the development of NASH in obese mice.
Methods.
Mice were fed a high fat diet (HFD) and obese animals were administered an HO-1 inducer with or without an inhibitor of HO activity to examine levels of adipose-derived NOV and possible links between increased synthesis of inflammatory adipokines and hepatic pathology.
Results.
NASH mice displayed decreased HO-1 levels and HO activity, increased levels of hepatic heme, NOV, MMP2, hepcidin, and increased NAS scores and hepatic fibrosis.
Increased HO-1 levels are associated with a decrease in NOV, improved hepatic NAS score, ameliorated fibrosis, and increases in mitochondrial integrity and insulin receptor phosphorylation.
Adipose tissue function is disrupted in obesity as evidenced by an increase in proinflammatory molecules such as NOV and a decrease in adiponectin.
Importantly, increased HO-1 levels are associated with a decrease of NOV, increased adiponectin levels, and increased levels of thermogenic and mitochondrial signaling associated genes in adipose tissue.
Conclusions.
These results suggest that the metabolic abnormalities in NASH are driven by decreased levels of hepatic HO-1 that is associated with an increase in the adipose-derived proinflammatory adipokine NOV in our obese mouse model of NASH.
Concurrently, induction of HO-1 provides protection against insulin resistance as seen by increased insulin receptor phosphorylation.
Pharmacological increases in HO-1 associated with decreases in NOV may offer a potential therapeutic approach in preventing fibrosis, mitochondrial dysfunction, and the development of NASH.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Sacerdoti, David& Singh, Shailendra P.& Schragenheim, Joseph& Bellner, Lars& Vanella, Luca& Raffaele, Marco…[et al.]. 2018. Development of NASH in Obese Mice is Confounded by Adipose Tissue Increase in Inflammatory NOV and Oxidative Stress. International Journal of Hepatology،Vol. 2018, no. 2018, pp.1-14.
https://search.emarefa.net/detail/BIM-1173050
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Sacerdoti, David…[et al.]. Development of NASH in Obese Mice is Confounded by Adipose Tissue Increase in Inflammatory NOV and Oxidative Stress. International Journal of Hepatology No. 2018 (2018), pp.1-14.
https://search.emarefa.net/detail/BIM-1173050
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Sacerdoti, David& Singh, Shailendra P.& Schragenheim, Joseph& Bellner, Lars& Vanella, Luca& Raffaele, Marco…[et al.]. Development of NASH in Obese Mice is Confounded by Adipose Tissue Increase in Inflammatory NOV and Oxidative Stress. International Journal of Hepatology. 2018. Vol. 2018, no. 2018, pp.1-14.
https://search.emarefa.net/detail/BIM-1173050
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1173050
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر