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  • 1
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    Upper intestinal lipids trigger a gut-brain-liver axis to regulate glucose production (2008)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2008-04-11
    Beschreibung: Energy and glucose homeostasis are regulated by food intake and liver glucose production, respectively. The upper intestine has a critical role in nutrient digestion and absorption. However, studies indicate that upper intestinal lipids inhibit food intake as well in rodents and humans by the activation of an intestine-brain axis. In parallel, a brain-liver axis has recently been proposed to detect blood lipids to inhibit glucose production in rodents. Thus, we tested the hypothesis that upper intestinal lipids activate an intestine-brain-liver neural axis to regulate glucose homeostasis. Here we demonstrate that direct administration of lipids into the upper intestine increased upper intestinal long-chain fatty acyl-coenzyme A (LCFA-CoA) levels and suppressed glucose production. Co-infusion of the acyl-CoA synthase inhibitor triacsin C or the anaesthetic tetracaine with duodenal lipids abolished the inhibition of glucose production, indicating that upper intestinal LCFA-CoAs regulate glucose production in the preabsorptive state. Subdiaphragmatic vagotomy or gut vagal deafferentation interrupts the neural connection between the gut and the brain, and blocks the ability of upper intestinal lipids to inhibit glucose production. Direct administration of the N-methyl-d-aspartate ion channel blocker MK-801 into the fourth ventricle or the nucleus of the solitary tract where gut sensory fibres terminate abolished the upper-intestinal-lipid-induced inhibition of glucose production. Finally, hepatic vagotomy negated the inhibitory effects of upper intestinal lipids on glucose production. These findings indicate that upper intestinal lipids activate an intestine-brain-liver neural axis to inhibit glucose production, and thereby reveal a previously unappreciated pathway that regulates glucose homeostasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Penny Y T -- Caspi, Liora -- Lam, Carol K L -- Chari, Madhu -- Li, Xiaosong -- Light, Peter E -- Gutierrez-Juarez, Roger -- Ang, Michelle -- Schwartz, Gary J -- Lam, Tony K T -- DK45024/DK/NIDDK NIH HHS/ -- DK47208/DK/NIDDK NIH HHS/ -- England -- Nature. 2008 Apr 24;452(7190):1012-6. doi: 10.1038/nature06852. Epub 2008 Apr 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Toronto General Hospital Research Institute, University Health Network, Toronto M5G 1L7, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18401341" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Acyl Coenzyme A/biosynthesis/metabolism ; Animals ; Brain/drug effects/*metabolism ; Dietary Fats/administration & dosage/metabolism/*pharmacology ; Fatty Acids/chemistry/metabolism ; Glucose/*biosynthesis/metabolism ; Homeostasis/drug effects ; Insulin/metabolism ; Intestines/drug effects/innervation/*metabolism ; *Lipid Metabolism ; Liver/drug effects/innervation/*metabolism ; Rats ; Satiety Response/drug effects ; Tetracaine/pharmacology ; Triazenes/pharmacology
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    The amphioxus genome and the evolution of the chordate karyotype (2008)
    Nature Publishing Group (NPG)
    Details
    Publikationsdatum: 2008-06-20
    Beschreibung: Lancelets ('amphioxus') are the modern survivors of an ancient chordate lineage, with a fossil record dating back to the Cambrian period. Here we describe the structure and gene content of the highly polymorphic approximately 520-megabase genome of the Florida lancelet Branchiostoma floridae, and analyse it in the context of chordate evolution. Whole-genome comparisons illuminate the murky relationships among the three chordate groups (tunicates, lancelets and vertebrates), and allow not only reconstruction of the gene complement of the last common chordate ancestor but also partial reconstruction of its genomic organization, as well as a description of two genome-wide duplications and subsequent reorganizations in the vertebrate lineage. These genome-scale events shaped the vertebrate genome and provided additional genetic variation for exploitation during vertebrate evolution.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Putnam, Nicholas H -- Butts, Thomas -- Ferrier, David E K -- Furlong, Rebecca F -- Hellsten, Uffe -- Kawashima, Takeshi -- Robinson-Rechavi, Marc -- Shoguchi, Eiichi -- Terry, Astrid -- Yu, Jr-Kai -- Benito-Gutierrez, E Lia -- Dubchak, Inna -- Garcia-Fernandez, Jordi -- Gibson-Brown, Jeremy J -- Grigoriev, Igor V -- Horton, Amy C -- de Jong, Pieter J -- Jurka, Jerzy -- Kapitonov, Vladimir V -- Kohara, Yuji -- Kuroki, Yoko -- Lindquist, Erika -- Lucas, Susan -- Osoegawa, Kazutoyo -- Pennacchio, Len A -- Salamov, Asaf A -- Satou, Yutaka -- Sauka-Spengler, Tatjana -- Schmutz, Jeremy -- Shin-I, Tadasu -- Toyoda, Atsushi -- Bronner-Fraser, Marianne -- Fujiyama, Asao -- Holland, Linda Z -- Holland, Peter W H -- Satoh, Nori -- Rokhsar, Daniel S -- BBS/B/12067/Biotechnology and Biological Sciences Research Council/United Kingdom -- BBS/B/12067/2/Biotechnology and Biological Sciences Research Council/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2008 Jun 19;453(7198):1064-71. doi: 10.1038/nature06967.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Energy Joint Genome Institute, Walnut Creek, California 94598, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18563158" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Chordata/classification/*genetics ; Conserved Sequence ; DNA Transposable Elements/genetics ; *Evolution, Molecular ; Gene Duplication ; Genes/genetics ; Genetic Linkage ; Genome/*genetics ; Humans ; Introns/genetics ; Karyotyping ; Multigene Family ; Phylogeny ; Polymorphism, Genetic/genetics ; Proteins/genetics ; Synteny ; Time Factors ; Vertebrates/classification/genetics
    Print ISSN: 0028-0836
    Digitale ISSN: 1476-4687
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von Nature Publishing Group (NPG)
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Regulation of blood glucose by hypothalamic pyruvate metabolism (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2005-08-06
    Beschreibung: The brain keenly depends on glucose for energy, and mammalians have redundant systems to control glucose production. An increase in circulating glucose inhibits glucose production in the liver, but this negative feedback is impaired in type 2 diabetes. Here we report that a primary increase in hypothalamic glucose levels lowers blood glucose through inhibition of glucose production in rats. The effect of glucose requires its conversion to lactate followed by stimulation of pyruvate metabolism, which leads to activation of adenosine triphosphate (ATP)-sensitive potassium channels. Thus, interventions designed to enhance the hypothalamic sensing of glucose may improve glucose homeostasis in diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lam, Tony K T -- Gutierrez-Juarez, Roger -- Pocai, Alessandro -- Rossetti, Luciano -- AG 21654/AG/NIA NIH HHS/ -- DK 20541/DK/NIDDK NIH HHS/ -- DK 45024/DK/NIDDK NIH HHS/ -- DK 48321/DK/NIDDK NIH HHS/ -- T32-AG023475/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2005 Aug 5;309(5736):943-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Medicine and Molecular Pharmacology, Diabetes Research Center, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16081739" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Astrocytes/metabolism ; Blood Glucose/*metabolism ; Citric Acid Cycle ; Feedback, Physiological ; Glucose/administration & dosage/*metabolism ; Glucose-6-Phosphatase/metabolism ; Hypothalamus/*metabolism ; Injections, Intraventricular ; Lactic Acid/metabolism ; Liver/*metabolism ; Male ; Neurons/metabolism ; Potassium Channels/metabolism ; Pyruvates/*metabolism ; Rats ; Rats, Sprague-Dawley
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    Proliferation of functional hair cells in vivo in the absence of the retinoblastoma protein (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2005-01-18
    Beschreibung: In mammals, hair cell loss causes irreversible hearing and balance impairment because hair cells are terminally differentiated and do not regenerate spontaneously. By profiling gene expression in developing mouse vestibular organs, we identified the retinoblastoma protein (pRb) as a candidate regulator of cell cycle exit in hair cells. Differentiated and functional mouse hair cells with a targeted deletion of Rb1 undergo mitosis, divide, and cycle, yet continue to become highly differentiated and functional. Moreover, acute loss of Rb1 in postnatal hair cells caused cell cycle reentry. Manipulation of the pRb pathway may ultimately lead to mammalian hair cell regeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sage, Cyrille -- Huang, Mingqian -- Karimi, Kambiz -- Gutierrez, Gabriel -- Vollrath, Melissa A -- Zhang, Duan-Sun -- Garcia-Anoveros, Jaime -- Hinds, Philip W -- Corwin, Jeffrey T -- Corey, David P -- Chen, Zheng-Yi -- DC-00200/DC/NIDCD NIH HHS/ -- DC-04546/DC/NIDCD NIH HHS/ -- DC-AG20208/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 18;307(5712):1114-8. Epub 2005 Jan 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurology Service, MGH-HMS Center for Nervous System Repair, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15653467" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Apoptosis ; Cell Count ; Cell Cycle ; Cell Differentiation ; *Cell Proliferation ; Cell Shape ; Cochlea/cytology/embryology ; Female ; Gene Deletion ; Gene Expression Profiling ; Genes, Retinoblastoma ; Hair Cells, Auditory, Inner/*cytology/*physiology ; Mice ; Mice, Knockout ; Mitosis ; Oligonucleotide Array Sequence Analysis ; Pregnancy ; Pyridinium Compounds/metabolism ; Quaternary Ammonium Compounds/metabolism ; Regeneration ; Retinoblastoma Protein/genetics/*physiology ; Saccule and Utricle/embryology/metabolism ; Stem Cells/cytology/physiology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Role of layer 6 of V2 visual cortex in object-recognition memory (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publikationsdatum: 2009-07-04
    Beschreibung: Cellular responses in the V2 secondary visual cortex to simple as well as complex visual stimuli have been well studied. However, the role of area V2 in visual memory remains unexplored. We found that layer 6 neurons of V2 are crucial for the processing of object-recognition memory (ORM). Using the protein regulator of G protein signaling-14 (RGS-14) as a tool, we found that the expression of this protein into layer 6 neurons of rat-brain area V2 promoted the conversion of a normal short-term ORM that normally lasts for 45 minutes into long-term memory detectable even after many months. Furthermore, elimination of the same-layer neurons by means of injection of a selective cytotoxin resulted in the complete loss of normal as well as protein-mediated enhanced ORM.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lopez-Aranda, Manuel F -- Lopez-Tellez, Juan F -- Navarro-Lobato, Irene -- Masmudi-Martin, Mariam -- Gutierrez, Antonia -- Khan, Zafar U -- New York, N.Y. -- Science. 2009 Jul 3;325(5936):87-9. doi: 10.1126/science.1170869.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neurobiology, Centro de Investigaciones Medico-Sanitarias, University of Malaga, Campus Teatinos s/n, 29071 Malaga, Spain. zkhan@uma.es〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19574389" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Lentivirus/genetics ; Memory/*physiology ; Memory, Short-Term/*physiology ; Neurons/physiology ; RGS Proteins/genetics/metabolism ; Rats ; Rats, Wistar ; Recognition (Psychology)/*physiology ; Temporal Lobe/physiology ; Visual Cortex/cytology/*physiology ; Visual Perception
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Publiziert von American Association for the Advancement of Science (AAAS)
    Standort Signatur Erwartet Verfügbarkeit
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