کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9879454 | 1534759 | 2005 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Transgenic mice overexpressing SREBP-1a under the control of the PEPCK promoter exhibit insulin resistance, but not diabetes
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کلمات کلیدی
SREBPinsulin tolerance testsIRS-22-Deoxy-glucoseSCAPHOMA-RNEFASREPEPCK2-DG - 2 DGIPGTT - IPGTivGTT - IVGTTLiver steatosis - استئاتوز کبدیNon-esterified fatty acid - اسید چرب غیر استرادیلیITT - اینجاInsulin receptor substrate-2 - زیر بغل گیرنده انسولین -2Transcription factor - عامل رونویسیphosphoenolpyruvate carboxykinase - فسفوآنولپیرود کربوکسیکینازlipodystrophy - لیپودیستروفی پیش رونده، لیپودیستروفیInsulin resistance - مقاومت به انسولین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Transgenic mice overexpressing SREBP-1a under the control of the PEPCK promoter exhibit insulin resistance, but not diabetes Transgenic mice overexpressing SREBP-1a under the control of the PEPCK promoter exhibit insulin resistance, but not diabetes](/preview/png/9879454.png)
چکیده انگلیسی
Sterol regulatory element-binding protein-1 (SREBP-1) is a transcription factor which regulates genes involved in the synthesis of fatty acids and triglycerides. The overexpression of nuclear SREBP-1a in transgenic mice under the control of the PEPCK promoter (TgSREBP-1a) caused a massively enlarged fatty liver and disappearance of peripheral white adipose tissue. In the current study, we estimated the impact of this lipid transcription factor on plasma glucose/insulin metabolism in vivo. TgSREBP-1a exhibited mild peripheral insulin resistance as evidenced by hyperinsulinemia both at fasting and after intravenous glucose loading, and retarded glucose reduction after insulin injection due to decreased plasma leptin levels. Intriguingly, hyperinsulinemia in TgSREBP-1a mice was markedly exacerbated in a fed state and sustained after intravenous glucose loading, and paradoxically decreased after the portal injection of glucose. TgSREBP-1a mice consistently showed very small plasma glucose increases after portal glucose loading because of a large capacity for hepatic glucose uptake. These data suggested that hepatic insulin resistance emerges postprandially. In addition, pancreatic islets from TgSREBP-1a were enlarged. These data demonstrate that SREBP-1a activation in the liver has a strong impact on plasma insulin levels, implicating the potential role of SREBPs in hepatic insulin metabolism relating to insulin resistance.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1740, Issue 3, 10 June 2005, Pages 427-433
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1740, Issue 3, 10 June 2005, Pages 427-433
نویسندگان
Akimitsu Takahashi, Hitoshi Shimano, Yoshimi Nakagawa, Takashi Yamamoto, Kaori Motomura, Takashi Matsuzaka, Hirohito Sone, Hiroaki Suzuki, Hideo Toyoshima, Nobuhiro Yamada,