The role of skeletal muscle insulin resistance in the pathogenesis of the metabolic syndrome.

The role of skeletal muscle insulin resistance in the pathogenesis of the metabolic syndrome. Research Abstract Details 

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The role of skeletal muscle insulin resistance in the pathogenesis of the metabolic syndrome. Abstract Text:

Kitt Falk Petersen,Sylvie Dufour,David B Savage,Stefan Bilz,Gina Solomon,Shin Yonemitsu,Gary W Cline,Douglas Befroy,Laura Zemany,Barbara B Kahn,Xenophon Papademetris,Douglas L Rothman,Gerald I Shulman,

We examined the hypothesis that insulin resistance in skeletal muscle promotes the development of atherogenic dyslipidemia, associated with the metabolic syndrome, by altering the distribution pattern of postprandial energy storage. Following ingestion of two high carbohydrate mixed meals, net muscle glycogen synthesis was reduced by approximately 60% in young, lean, insulin-resistant subjects compared with a similar cohort of age-weight-body mass index-activity-matched, insulin-sensitive, control subjects. In contrast, hepatic de novo lipogenesis and hepatic triglyceride synthesis were both increased by >2-fold in the insulin-resistant subjects. These changes were associated with a 60% increase in plasma triglyceride concentrations and an approximately 20% reduction in plasma high-density lipoprotein concentrations but no differences in plasma concentrations of TNF-alpha, IL-6, adiponectin, resistin, retinol binding protein-4, or intraabdominal fat volume. These data demonstrate that insulin resistance in skeletal muscle, due to decreased muscle glycogen synthesis, can promote atherogenic dyslipidemia by changing the pattern of ingested carbohydrate away from skeletal muscle glycogen synthesis into hepatic de novo lipogenesis, resulting in an increase in plasma triglyceride concentrations and a reduction in plasma high-density lipoprotein concentrations. Furthermore, insulin resistance in these subjects was independent of changes in the plasma concentrations of TNF-alpha, IL-6, high-molecular-weight adiponectin, resistin, retinol binding protein-4, or intraabdominal obesity, suggesting that these factors do not play a primary role in causing insulin resistance in the early stages of the metabolic syndrome.

The role of skeletal muscle insulin resistance in the pathogenesis of the metabolic syndrome. Publishing Authors By Initials

KF Petersen,S Dufour,DB Savage,S Bilz,G Solomon,S Yonemitsu,GW Cline,D Befroy,L Zemany,BB Kahn,X Papademetris,DL Rothman,GI Shulman,

For similar musculoskeletal system: muscles: muscle, skeletal research abstracts see: musculoskeletal system: muscles: muscle, skeletal research

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MEDLINE DATE:

The role of skeletal muscle insulin resistance in the pathogenesis of the metabolic syndrome. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Proceedings of the National Academy of Sciences of

VOLUME: 104

Page Numbers: 12587-94

Journal Abbreviation: Proc. Natl. Acad. Sci. U.S.A.

ISSN: 0027-8424

DAY: 18

MONTH: 07

YEAR: 2007

The role of skeletal muscle insulin resistance in the pathogenesis of the metabolic syndrome. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 7505876

The role of skeletal muscle insulin resistance in the pathogenesis of the metabolic syndrome. Keywords Mesh Terms:

KEYWORDS: Muscle, Skeletal

MESH TERMS: metabolism

Chemical & Substance for Abstract: The role of skeletal muscle insulin resistance in the pathogenesis of the metabolic syndrome. Information

Substance Name: Glycogen

Registry Number: 9005-79-2

Grant and Affiliation Information for The role of skeletal muscle insulin resistance in the pathogenesis of the metabolic syndrome.

AFFILIATION: Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06536, USA.

Country: United States

AGENCY: United States NIBIB

GRANT: R01 EB 006494

ACRONYM: EB

MEDLINETA: Proc Natl Acad Sci U S A

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