دورية أكاديمية

Islet adaptation to obesity and insulin resistance in WNIN/GR-Ob rats.

التفاصيل البيبلوغرافية
العنوان: Islet adaptation to obesity and insulin resistance in WNIN/GR-Ob rats.
المؤلفون: Singh H; a Biochemistry/Stem Cell Research; National Institute of Nutrition; Indian Council of Medical Research ; Hyderabad , India., Ganneru S, Malakapalli V, Chalasani M, Nappanveettil G, Bhonde RR, Venkatesan V
المصدر: Islets [Islets] 2014; Vol. 6 (5-6), pp. e998099.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Taylor & Francis Country of Publication: United States NLM ID: 101495366 Publication Model: Print Cited Medium: Internet ISSN: 1938-2022 (Electronic) Linking ISSN: 19382014 NLM ISO Abbreviation: Islets Subsets: MEDLINE
أسماء مطبوعة: Publication: 2015- : Philapdelphia, PA : Taylor & Francis
Original Publication: Austin, TX : Landes Bioscience
مواضيع طبية MeSH: Insulin Resistance/*physiology , Islets of Langerhans/*physiopathology , Obesity/*physiopathology, Adaptation, Physiological/physiology ; Age Factors ; Animals ; Body Weight ; Female ; Gene Expression/physiology ; Glucagon/metabolism ; Insulin/metabolism ; Insulin-Secreting Cells/pathology ; Insulin-Secreting Cells/physiology ; Islets of Langerhans/cytology ; Islets of Langerhans/pathology ; Islets of Langerhans/ultrastructure ; Microscopy, Electron, Scanning ; Organ Size ; Oxidative Stress/physiology ; Rats ; Rats, Mutant Strains/physiology ; Somatostatin/metabolism
مستخلص: WNIN/GR-Ob mutant rat is a novel animal model to study metabolic syndrome (obesity, insulin resistance, hyperinsulinemia, impaired glucose tolerance and cardiovascular diseases). We have investigated the islet characteristics of obese mutants at different age groups (1, 6 and 12 months) to assess the islet changes in response to early and chronic metabolic stress. Our data demonstrates altered islet cell morphology and function (hypertrophy, fibrotic lesions, vacuolation, decreased stimulation index, increased TNFα, ROS and TBARS levels) in mutants as compared to controls. Furthermore, network analysis (gene-gene interaction) studied in pancreas demonstrated increased inflammation as a key factor underlying obesity/metabolic syndrome in mutants. These observations pave way to explore this model to understand islet adaptation in response to metabolic syndrome.
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فهرسة مساهمة: Keywords: ANOVA, one-way analysis of variance; BM-MSCs, bone marrow derived mesenchymal stem cells; DAPI, 4′,6-diamidino-2-phenylindol; DTZ, Dithizone; FBG, fasting blood glucose; H&E, hematoxylin and eosin stain; HI, hyperinsulinemia; HOMA-IR, homeostatic model assessment for insulin resistance; IGT, impaired glucose tolerance; IHC, immunohistochemistry; IR, insulin resistance; KRBH, krebs ringer bicarbonate; MS, metabolic syndrome; NCLAS, National Center for Laboratory Animal Sciences; NIN, National Institute of Nutrition; PBS, phosphate buffered saline; ROS, reactive oxygen species; SEM, scanning electron microscope; T2D, type 2 diabetes; TBARS, thiobarbituric acid reactive substances; TEM, transmission electron microscopy; TNFα, tumor necrosis factors; WNIN, Wistar rats raised at National Institute of Nutrition; WNIN/GR-Ob mutant rats; hyperinsulinemia; hypertrophy; insulin resistance; islets
المشرفين على المادة: 0 (Insulin)
51110-01-1 (Somatostatin)
9007-92-5 (Glucagon)
تواريخ الأحداث: Date Created: 20150403 Date Completed: 20151127 Latest Revision: 20190108
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC4398287
DOI: 10.1080/19382014.2014.998099
PMID: 25833252
قاعدة البيانات: MEDLINE
الوصف
تدمد:1938-2022
DOI:10.1080/19382014.2014.998099