ER Stress Inhibits Liver Fatty Acid Oxidation while Unmitigated Stress Leads to Anorexia-Induced Lipolysis and Both Liver and Kidney Steatosis

التفاصيل البيبلوغرافية
العنوان: ER Stress Inhibits Liver Fatty Acid Oxidation while Unmitigated Stress Leads to Anorexia-Induced Lipolysis and Both Liver and Kidney Steatosis
المؤلفون: Eric B. Taylor, Deng-Fu Guo, Diane DeZwaan-McCabe, Michelle C. Gorecki, Matthew P. Gillum, D. Thomas Rutkowski, Lynn M. Teesch, Ryan D. Sheldon, Kamal Rahmouni, Randal J. Kaufman, Erica R. Gansemer
المصدر: Cell Reports, Vol 19, Iss 9, Pp 1794-1806 (2017)
DeZwaan-McCabe, D, Sheldon, R D, Gorecki, M C, Guo, D-F, Gansemer, E R, Kaufman, R J, Rahmouni, K, Gillum, M P, Taylor, E B, Teesch, L M & Rutkowski, D T 2017, ' ER Stress Inhibits Liver Fatty Acid Oxidation while Unmitigated Stress Leads to Anorexia-Induced Lipolysis and Both Liver and Kidney Steatosis ', Cell Reports, vol. 19, no. 9, pp. 1794-1806 . https://doi.org/10.1016/j.celrep.2017.05.020Test
بيانات النشر: Elsevier, 2017.
سنة النشر: 2017
مصطلحات موضوعية: 0301 basic medicine, medicine.medical_specialty, Biology, Kidney, Article, General Biochemistry, Genetics and Molecular Biology, Mice, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Journal Article, medicine, Animals, Lipolysis, Beta oxidation, lcsh:QH301-705.5, fatty acid oxidation, fatty liver, chemistry.chemical_classification, Tunicamycin, Endoplasmic reticulum, Fatty Acids, Renal steatosis, Fatty liver, Fatty acid, fatty kidney, unfolded protein response, Endoplasmic Reticulum Stress, medicine.disease, Lipids, Activating Transcription Factor 6, Anorexia, Mice, Inbred C57BL, 030104 developmental biology, Endocrinology, Adipose Tissue, Liver, chemistry, lcsh:Biology (General), 030220 oncology & carcinogenesis, Unfolded protein response, lipolysis, lipidomics, Steatosis, ER stress, Oxidation-Reduction
الوصف: The unfolded protein response (UPR), induced by endoplasmic reticulum (ER) stress, regulates the expression of factors that restore protein folding homeostasis. However, in the liver and kidney, ER stress also leads to lipid accumulation, accompanied at least in the liver by transcriptional suppression of metabolic genes. The mechanisms of this accumulation, including which pathways contribute to the phenotype in each organ, are unclear. We combined gene expression profiling, biochemical assays, and untargeted lipidomics to understand the basis of stress-dependent lipid accumulation, taking advantage of enhanced hepatic and renal steatosis in mice lacking the ER stress sensor ATF6α. We found that impaired fatty acid oxidation contributed to the early development of steatosis in the liver but not the kidney, while anorexia-induced lipolysis promoted late triglyceride and free fatty acid accumulation in both organs. These findings provide evidence for both direct and indirect regulation of peripheral metabolism by ER stress.
وصف الملف: application/pdf
اللغة: English
تدمد: 2211-1247
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::822c4b566bd5e70677ebbfba910f4809Test
http://www.sciencedirect.com/science/article/pii/S2211124717306459Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....822c4b566bd5e70677ebbfba910f4809
قاعدة البيانات: OpenAIRE