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Tissue-specific expression and regulation of GSK-3 in human skeletal muscle and adipose tissue.

Tissue-specific expression and regulation of GSK-3 in human skeletal muscle and adipose tissue. Research Abstract Details 

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  • Tissue-specific expression and regulation of GSK-3 in human skeletal muscle and adipose tissue. Abstract Text:

    theodore p ciaraldiTheodore P Ciaraldi,deborah k ohDeborah K Oh,louis christiansenLouis Christiansen,svetlana e nikoulinaSvetlana E Nikoulina,alice p s kongAlice P S Kong,sunita baxiSunita Baxi,sunder mudaliarSunder Mudaliar,robert r henryRobert R Henry,

    Glycogen synthase kinase-3 (GSK-3) is a ubiquitous kinase implicated in both insulin action and adipogenesis. To determine how these multiple roles may relate to insulin resistance, we studied the regulation of GSK-3 protein expression and phosphorylation in skeletal muscle and isolated adipocytes from nonobese healthy control (HC), obese control (OC), and obese type 2 diabetic (OT2D) subjects. At baseline there were no differences in the GSK-3 protein expression in adipocytes. OC subjects underwent a 6-mo caloric restriction resulting in a 7% decrease in body mass index (BMI) and a 21% improvement in insulin-stimulated whole body glucose disposal rate (GDR). GSK-3alpha and GSK-3beta expression decreased in adipocytes (P < 0.05), whereas GSK-3alpha protein expression increased in skeletal muscle (P < 0.05). OT2D subjects were treated with troglitazone or metformin for 3-4 mo. After troglitazone treatment GDR improved (P < 0.05) despite an increase in BMI (P < 0.05), whereas metformin had no significant effect on GDR. There was no significant change in GSK-3 expression in adipocytes following troglitazone, whereas both GSK-3alpha and -beta were decreased in skeletal muscle (P < 0.05). Metformin treatment had no significant impact on GSK-3 protein expression in either adipocytes or skeletal muscle. Neither treatment influenced GSK-3 serine phosphorylation in skeletal muscle or adipocytes. These results suggest that there is tissue specificity for the regulation of GSK-3 in humans. In skeletal muscle GSK-3 plays a role in control of metabolism and insulin action, whereas the function in adipose tissue is less clear.

    Tissue-specific expression and regulation of GSK-3 in human skeletal muscle and adipose tissue. Publishing Authors By Initials

    tp ciaraldiTP Ciaraldi,dk ohDK Oh,l christiansenL Christiansen,se nikoulinaSE Nikoulina,ap kongAP Kong,s baxiS Baxi,s mudaliarS Mudaliar,rr henryRR Henry,

    For similar pathological conditions, signs and symptoms: signs and symptoms: body weight: body weight changes: weight loss research abstracts see: pathological conditions, signs and symptoms: signs and symptoms: body weight: body weight changes: weight loss research

    PUBMED ID PMID:

    MEDLINE DATE:

    Tissue-specific expression and regulation of GSK-3 in human skeletal muscle and adipose tissue. Journal Published:

    PUBLICATION TYPE: Research Support, U.S. Gov't,

    Journal: American journal of physiology. Endocrinology and

    VOLUME: 291

    Page Numbers: E891-8

    Journal Abbreviation: Am. J. Physiol. Endocrinol. Me

    ISSN: 0193-1849

    DAY: 6

    MONTH: 06

    YEAR: 2006

    Tissue-specific expression and regulation of GSK-3 in human skeletal muscle and adipose tissue. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 100901226

    Tissue-specific expression and regulation of GSK-3 in human skeletal muscle and adipose tissue. Keywords Mesh Terms:

    KEYWORDS: Weight Loss

    MESH TERMS: administration & dosage

    Chemical & Substance for Abstract: Tissue-specific expression and regulation of GSK-3 in human skeletal muscle and adipose tissue. Information

    Substance Name: glycogen synthase kinase 3 beta

    Registry Number: EC 2.7.1.37

    Grant and Affiliation Information for Tissue-specific expression and regulation of GSK-3 in human skeletal muscle and adipose tissue.

    AFFILIATION: Veterans Affairs San Diego Healthcare System, San Diego, CA 92161, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIDDK

    GRANT: R01-DK-258291

    ACRONYM: DK

    MEDLINETA: Am J Physiol Endocrinol Metab

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