Muscle-specific deletion of rictor impairs insulin-stimulated glucose transport and enhances Basal glycogen synthase activity.

Muscle-specific deletion of rictor impairs insulin-stimulated glucose transport and enhances Basal glycogen synthase activity. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Muscle-specific deletion of rictor impairs insulin-stimulated glucose transport and enhances Basal glycogen synthase activity. Abstract Text:

Anil Kumar,Thurl E Harris,Susanna R Keller,Kin M Choi,Mark A Magnuson,John C Lawrence,Anil Kumar,Thurl E Harris,Susanna R Keller,Kin M Choi,Mark A Magnuson,John C Lawrence,Anil Kumar,Thurl E Harris,Susanna R Keller,Kin M Choi,Mark A Magnuson,John C Lawrence,

Rictor is an essential component of mTOR (mammalian target of rapamycin) complex 2 (mTORC2), a kinase complex that phosphorylates Akt at Ser473 upon activation of phosphatidylinositol 3-kinase (PI-3 kinase). Since little is known about the role of either rictor or mTORC2 in PI-3 kinase-mediated physiological processes in adult animals, we generated muscle-specific rictor knockout mice. Muscle from male rictor knockout mice exhibited decreased insulin-stimulated glucose uptake, and the mice showed glucose intolerance. In muscle lacking rictor, the phosphorylation of Akt at Ser473 was reduced dramatically in response to insulin. Furthermore, insulin-stimulated phosphorylation of the Akt substrate AS160 at Thr642 was reduced in rictor knockout muscle, indicating a defect in insulin signaling to stimulate glucose transport. However, the phosphorylation of Akt at Thr308 was normal and sufficient to mediate the phosphorylation of glycogen synthase kinase 3 (GSK-3). Basal glycogen synthase activity in muscle lacking rictor was increased to that of insulin-stimulated controls. Consistent with this, we observed a decrease in basal levels of phosphorylated glycogen synthase at a GSK-3/protein phosphatase 1 (PP1)-regulated site in rictor knockout muscle. This change in glycogen synthase phosphorylation was associated with an increase in the catalytic activity of glycogen-associated PP1 but not increased GSK-3 inactivation. Thus, rictor in muscle tissue contributes to glucose homeostasis by positively regulating insulin-stimulated glucose uptake and negatively regulating basal glycogen synthase activity.

Muscle-specific deletion of rictor impairs insulin-stimulated glucose transport and enhances Basal glycogen synthase activity. Publishing Authors By Initials

A Kumar,TE Harris,SR Keller,KM Choi,MA Magnuson,JC Lawrence,A Kumar,TE Harris,SR Keller,KM Choi,MA Magnuson,JC Lawrence,A Kumar,TE Harris,SR Keller,KM Choi,MA Magnuson,JC Lawrence,

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE:

Muscle-specific deletion of rictor impairs insulin-stimulated glucose transport and enhances Basal glycogen synthase activity. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Molecular and cellular biology

VOLUME: 28

Page Numbers: 61-70

Journal Abbreviation: Mol. Cell. Biol.

ISSN: 1098-5549

DAY: 29

MONTH: 10

YEAR: 2007

Muscle-specific deletion of rictor impairs insulin-stimulated glucose transport and enhances Basal glycogen synthase activity. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8109087

Muscle-specific deletion of rictor impairs insulin-stimulated glucose transport and enhances Basal glycogen synthase activity. Keywords Mesh Terms:

KEYWORDS:

MESH TERMS:

Chemical & Substance for Abstract: Muscle-specific deletion of rictor impairs insulin-stimulated glucose transport and enhances Basal glycogen synthase activity. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for Muscle-specific deletion of rictor impairs insulin-stimulated glucose transport and enhances Basal glycogen synthase activity.

AFFILIATION: Department of Pharmacology, University of Virginia Health System, P.O. Box 800735, 1300 Jefferson Park Ave., Charlottesville, VA 22908, USA. al4p@virginia.edu

Country: United States

AGENCY:

GRANT:

ACRONYM:

MEDLINETA: Mol Cell Biol

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Muscle-specific deletion of rictor impairs insulin-stimulated glucose transport and enhances Basal glycogen synthase activity Related Publications

• A pilot study of [18F]fluorodeoxyglucose positron emission tomography scans during and after radiation-based therapy in patients with non small-cell lung cancer.
• Acquisition of a "Group A"-selective Src kinase inhibitor via a global targeting strategy.
• An Impulse-Response Model using Pace and Duration Correlates to Performance of a 1500 m Olympic Finalist: 1416: Board #179 May 30 11:00 AM -12:30 PM.
• An evaluation of the seasonality of veterinary treatments for lameness in UK dairy cattle.
• Analysis of the thiol status of peripheral blood leukocytes in rheumatoid arthritis patients.
• Aryl hydrocarbon receptor activation during influenza virus infection unveils a novel pathway of IFN-gamma production by phagocytic cells.
• BRCA1 does not paint the inactive X to localize XIST RNA but may contribute to broad changes in cancer that impact XIST and Xi heterochromatin.
• BRCA1 foci in normal S-phase nuclei are linked to interphase centromeres and replication of pericentric heterochromatin.
• Central overexpression of angiotensin AT(1A) receptors prevents dopamine D(2) receptor regulation of alcohol consumption in mice.
• Cr04 six year, prospective analysis of rectal bleeding clinics at the queen elizabeth hospital, adelaide, South australia.
• Environmental toxins as modulators of antiviral immune responses.
• Evidence that the Pim1 kinase gene is a direct target of HOXA9.
• Heartbeat perception in depression.
• Housing system, milk production, and zero-grazing effects on lameness and leg injury in dairy cows.
• Identification of a novel targeting sequence for regulated secretion in the serine protease inhibitor neuroserpin.
• Insulin controls subcellular localization and multisite phosphorylation of the phosphatidic acid phosphatase, lipin 1.
• Lead effects on development and function of bone marrow-derived dendritic cells promote Th2 immune responses.
• Light-regulated sampling of protein tyrosine kinase activity.
• Mechanism of inactivation of plasminogen activator inhibitor-1 by a small molecule inhibitor.
• Open access publication is growing in importance.
• PRAS40 regulates mTORC1 kinase activity by functioning as a direct inhibitor of substrate binding.
• Propagating uncertainty in microarray data analysis.
• Protection against lethal challenge with Streptococcus pneumoniae is conferred by aryl hydrocarbon receptor activation but is not associated with an enhanced inflammatory response.
• Sterols of Delphinium ajacis; Production and Metabolic Relationships in Whole Plants and Callus Tissue*.
• The Gibbs Centroid Sampler.
• The clinical application of intensity-modulated radiation therapy.
• The contributions of integrin affinity and integrin-cytoskeletal engagement in endothelial and smooth muscle cell adhesion to vitronectin.
• The extent and severity of vascular leakage as evidence of tumor aggressiveness in high-grade gliomas.
• Twinning in mares: A survey of veterinarians and analyses of theriogenology records.
• Wettability modification and the subsequent manipulation of protein adsorption on a Ti6Al4V alloy by means of CO2 laser surface treatment.