دورية أكاديمية

The obesity and nonalcoholic fatty liver disease mouse model revisited: Liver oxidative stress, hepatocyte apoptosis, and proliferation.

التفاصيل البيبلوغرافية
العنوان: The obesity and nonalcoholic fatty liver disease mouse model revisited: Liver oxidative stress, hepatocyte apoptosis, and proliferation.
المؤلفون: Reis-Barbosa PH; Laboratory of Morphometry, Metabolism, and Cardiovascular Diseases, The University of the State of Rio de Janeiro, Rio de Janeiro, RJ, Brazil; Laboratory of Ultrastructure and Tissue Biology, Biomedical Center, Institute of Biology, The University of the State of Rio de Janeiro, Rio de Janeiro, RJ, Brazil. Electronic address: barbosaphr@outlook.com., Marinho TS; Laboratory of Morphometry, Metabolism, and Cardiovascular Diseases, The University of the State of Rio de Janeiro, Rio de Janeiro, RJ, Brazil. Electronic address: thatymarinho@gmail.com., Matsuura C; Department of Pharmacology, The University of the State of Rio de Janeiro, Rio de Janeiro, RJ, Brazil. Electronic address: crismatsuura@gmail.com., Aguila MB; Laboratory of Morphometry, Metabolism, and Cardiovascular Diseases, The University of the State of Rio de Janeiro, Rio de Janeiro, RJ, Brazil. Electronic address: mbaguila@uerj.br., de Carvalho JJ; Laboratory of Ultrastructure and Tissue Biology, Biomedical Center, Institute of Biology, The University of the State of Rio de Janeiro, Rio de Janeiro, RJ, Brazil. Electronic address: carvalho.jj@bol.com.br., Mandarim-de-Lacerda CA; Laboratory of Morphometry, Metabolism, and Cardiovascular Diseases, The University of the State of Rio de Janeiro, Rio de Janeiro, RJ, Brazil. Electronic address: mandarim@uerj.br.
المصدر: Acta histochemica [Acta Histochem] 2022 Oct; Vol. 124 (7), pp. 151937. Date of Electronic Publication: 2022 Aug 08.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Gustav Fischer Verlag Country of Publication: Germany NLM ID: 0370320 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1618-0372 (Electronic) Linking ISSN: 00651281 NLM ISO Abbreviation: Acta Histochem Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Jena Gustav Fischer Verlag
مواضيع طبية MeSH: Insulins*/metabolism , Non-alcoholic Fatty Liver Disease*, Animals ; Apoptosis ; Caspase 3/metabolism ; Cell Proliferation ; Diet, High-Fat/adverse effects ; Disease Models, Animal ; Glucose/metabolism ; Hepatocytes/metabolism ; Humans ; Infant ; Liver/metabolism ; Male ; Mice ; Obesity/metabolism ; Oxidative Stress ; Proliferating Cell Nuclear Antigen/metabolism
مستخلص: The study revisited the diet-induced obesity (DIO) mice and the nonalcoholic fatty liver disease (NAFLD) pathogenesis to serve as a translational model. Hepatic beta-oxidation pathways, lipogenesis, oxidative stress, hepatocyte apoptosis, and proliferation were investigated in obese mice. Three-month-old male mice were divided according to their diet for fifteen weeks, the control diet (C group, containing 10% energy from fat) and the high-fat diet (HF group, containing 50% energy from fat). Body weight (BW), liver mass, and steatosis were higher in the HF group than in the C group. Also, gene expression related to beta-oxidation and lipogenesis showed an adverse profile, and insulin and glucose signaling pathways were impaired in the HF group compared to the C group. As a result, steatosis was prevalent in the HF group but not in the C group. Furthermore, the pathways that generate NAFLD were negatively modulated by oxidative stress in the HF animals than in the C ones. The caspase 3 immunolabeled HF hepatocytes with increased gene and protein expressions related to apoptosis while proliferating cell nuclear antigen labeled C hepatocytes. In conclusion, the findings in the DIO mouse model reproduce the NAFLD profile relative to the human NAFLD's apoptosis, insulin signaling, lipogenesis, beta-oxidation, and oxidative stress. Therefore, the model is adequate for a translational perspective's morphological, biochemical, and molecular research on NAFLD.
Competing Interests: Conflicts of interest The authors disclose that they have no financial interest or commercial sponsor for this work.
(Copyright © 2022 Elsevier GmbH. All rights reserved.)
فهرسة مساهمة: Keywords: Animal model; High-fat diet; Mice; Non-alcoholic fatty liver disease; Obesity
المشرفين على المادة: 0 (Insulins)
0 (Proliferating Cell Nuclear Antigen)
EC 3.4.22.- (Caspase 3)
IY9XDZ35W2 (Glucose)
تواريخ الأحداث: Date Created: 20220811 Date Completed: 20221013 Latest Revision: 20221017
رمز التحديث: 20221213
DOI: 10.1016/j.acthis.2022.151937
PMID: 35952484
قاعدة البيانات: MEDLINE
الوصف
تدمد:1618-0372
DOI:10.1016/j.acthis.2022.151937