کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8477238 | 1550895 | 2014 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Toxicity generated through inhibition of pyruvate carboxylase and carnitine palmitoyl transferase-1 is similar to high glucose/palmitate-induced glucolipotoxicity in INS-1 beta cells
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کلمات کلیدی
OxaloacetatePPARPKCOLETFTCACPT-1AnaplerosisOAAPAAEToetomoxirJnkAMPKAMP-activated protein kinase - AMP-پروتئین کیناز فعال شده استC/EBP homologous protein - C / EBP پروتئین همولوگc-Jun N-terminal kinase - C-Jun N-terminal kinaseROS - ROSEndoplasmic reticulum (ER) stress - استرس اندوتلیوم رتیکولوم (ER)Sprague Dawley - اسپراگ داولیtricarboxylic acid - اسید تری کربوکسیلیکPhenylacetic acid - اسید فینسیلیکFatty acid oxidation - اکسیداسیون اسید چربCHOP - تکه کردنdiacylglycerol - دیسیل گلیسیرینDAG - روزGlucolipotoxicity - سمیت گلوکسیتendoplasmic reticulum - شبکه آندوپلاسمی FAO - فائوProtein kinase C - پروتئین کیناز سیpyruvate carboxylase - پیرووات کربوکسیلازReactive oxygen species - گونههای فعال اکسیژنperoxisome proliferator-activated receptor - گیرنده فعال فعال پروکسیوم
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Toxicity generated through inhibition of pyruvate carboxylase and carnitine palmitoyl transferase-1 is similar to high glucose/palmitate-induced glucolipotoxicity in INS-1 beta cells Toxicity generated through inhibition of pyruvate carboxylase and carnitine palmitoyl transferase-1 is similar to high glucose/palmitate-induced glucolipotoxicity in INS-1 beta cells](/preview/png/8477238.png)
چکیده انگلیسی
This work was initiated to determine whether toxicity generated through inhibition of mitochondrial fuel metabolism is similar to high glucose/palmitate (HG/PA)-induced glucolipotoxicity. Influx of glucose and free fatty acids into the tricarboxylic acid (TCA) cycle was inhibited by treatment with the pyruvate carboxylase (PC) inhibitor phenylacetic acid (PAA) and carnitine palmitoyl transferase-1 (CPT-1) inhibitor etomoxir (Eto), or knockdown of PC and CPT-1. Treatment of PAA/Eto or knockdown of PC/CPT-1 induced apoptotic death in INS-1 beta cells. Similar to HG/PA treatment, PAA/Eto increased endoplasmic reticulum stress responses but decreased the Akt signal. JNK inhibitor or chemical chaperone was protective against both PAA/Eto- and HG/PA-induced cell death. All attempts to reduce [Ca2+]i, stimulate lipid metabolism, and increase the TCA cycle intermediate pool protected PAA/Eto-induced death as well as HG/PA-induced death. These data suggest that signals induced from impaired mitochondrial fuel metabolism play a critical role in HG/PA-induced glucolipotoxicity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Endocrinology - Volume 383, Issues 1â2, 5 March 2014, Pages 48-59
Journal: Molecular and Cellular Endocrinology - Volume 383, Issues 1â2, 5 March 2014, Pages 48-59
نویسندگان
Ji-Hyun Lee, Ik-Rak Jung, Sung-E Choi, Sung-Mi Lee, Soo-Jin Lee, Seung Jin Han, Hae Jin Kim, Dae Jung Kim, Kwan-Woo Lee, Yup Kang,