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Content Provider | World Health Organization (WHO)-Global Index Medicus |
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Author | Khuder, Saja S. Sanchez, Edwin R. Al-share, Qusai Y. Mopidevi, Brahma R. Ramakrishnan, Sadeesh K. Abdallah, Simon L. Russo, Lucia Muturi, Harrison T. Najjar, Sonia M. Patel, Payal R. Shah, Yatrik M. Heinrich, Garrett Oyarce, Ana Maria |
Description | Author Affiliation: Ramakrishnan SK ( From the Center for Diabetes and Endocrine Research and Department of Physiology and Pharmacology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, Ohio 43614.); Khuder SS ( From the Center for Diabetes and Endocrine Research and Department of Physiology and Pharmacology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, Ohio 43614.); Al-Share QY ( From the Center for Diabetes and Endocrine Research and Department of Physiology and Pharmacology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, Ohio 43614.); Russo L ( From the Center for Diabetes and Endocrine Research and Department of Physiology and Pharmacology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, Ohio 43614.); Abdallah SL ( From the Center for Diabetes and Endocrine Research and Department of Physiology and Pharmacology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, Ohio 43614.); Patel PR ( From the Center for Diabetes and Endocrine Research and Department of Physiology and Pharmacology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, Ohio 43614.); Heinrich G ( From the Center for Diabetes and Endocrine Research and Department of Physiology and Pharmacology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, Ohio 43614.); Muturi HT ( From the Center for Diabetes and Endocrine Research and Department of Physiology and Pharmacology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, Ohio 43614.); Mopidevi BR ( Department of Physiology and Pharmacology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, Ohio 43614.); Oyarce AM ( From the Center for Diabetes and Endocrine Research and Department of Physiology and Pharmacology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, Ohio 43614.); Shah YM ( Departments of Internal Medicine, Division of Gastroenterology and Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan 48109, and.); Sanchez ER ( From the Center for Diabetes and Endocrine Research and Department of Physiology and Pharmacology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, Ohio 43614.); Najjar SM ( From the Center for Diabetes and Endocrine Research and Department of Physiology and Pharmacology, College of Medicine and Life Sciences, University of Toledo, Health Science Campus, Toledo, Ohio 43614, Department of Biomedical Sciences, Heritage College of Osteopathic Medicine, Ohio University, Ath) |
Abstract | Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is expressed at high levels in the hepatocyte, consistent with its role in promoting insulin clearance in liver. CEACAM1 also mediates a negative acute effect of insulin on fatty acid synthase activity. Western blot analysis reveals lower hepatic CEACAM1 expression during fasting. Treating of rat hepatoma FAO cells with Wy14,643, an agonist of peroxisome proliferator-activated receptor (PPAR ), rapidly reduces Ceacam1 mRNA and CEACAM1 protein levels within 1 and 2 h, respectively. Luciferase reporter assay shows a decrease in the promoter activity of both rat and mouse genes by Ppar activation, and 5'-deletion and block substitution analyses reveal that the Ppar response element between nucleotides -557 and -543 is required for regulation of the mouse promoter activity. Chromatin immunoprecipitation analysis demonstrates binding of liganded Ppar toCeacam1promoter in liver lysates ofPpar (+/+), but notPpar (-/-)mice fed a Wy14,643-supplemented chow diet. Consequently, Wy14,643 feeding reduces hepatic Ceacam1 mRNA and CEACAM1 protein levels, thus decreasing insulin clearance to compensate for compromised insulin secretion and maintain glucose homeostasis and insulin sensitivity in wild-type mice. Together, the data show that the low hepatic CEACAM1 expression at fasting is mediated by Ppar -dependent mechanisms. Changes in CEACAM1 expression contribute to the coordination of fatty acid oxidation and insulin action in the fasting-refeeding transition. |
ISSN | 00219258 |
e-ISSN | 1083351X |
Journal | Journal of Biological Chemistry |
Issue Number | 15 |
Volume Number | 291 |
Language | English |
Publisher | American Society for Biochemistry and Molecular Biology (United States) |
Publisher Date | 2016-04-08 |
Publisher Place | United States |
Access Restriction | Open |
Subject Keyword | Antigens, CD Genetics Cell Adhesion Molecules Fasting Fatty Acids Metabolism Gene Expression Regulation Liver PPAR Alpha Animals Cells, Cultured Gene Deletion Insulin Mice Mice, Inbred C57BL Oxidation-Reduction Promoter Regions, Genetic RNA, Messenger Research Support, N.I.H., Extramural Biochemistry Molecular Biology |
Content Type | Text |
Resource Type | Article |
Subject | Molecular Biology Cell Biology Biochemistry |
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