Impaired TCA cycle flux in mitochondria in skeletal muscle from type 2 diabetic subjects

Marker or maker of the diabetic phenotype?

Michael Gaster, Jan O Nehlin, Ariane D Minet

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Resumé

The diabetic phenotype is complex, requiring elucidation of key initiating defects. Recent research has shown that diabetic myotubes express a primary reduced tricarboxylic acid (TCA) cycle flux. A reduced TCA cycle flux has also been shown both in insulin resistant offspring of T2D patients and exercising T2D patients in vivo. This review will discuss the latest advances in the understanding of the molecular mechanisms regulating the TCA cycle with focus on possible underlying mechanism which could explain the impaired TCA flux in insulin resistant human skeletal muscle in type 2 diabetes. A reduced TCA is both a marker and a maker of the diabetic phenotype.
OriginalsprogEngelsk
TidsskriftArchives of Physiology and Biochemistry
Vol/bind118
Udgave nummer3
Sider (fra-til)156-89
Antal sider34
ISSN1381-3455
DOI
StatusUdgivet - 2012

Fingeraftryk

Citric Acid Cycle
Skeletal Muscle
Insulin
Type 2 Diabetes Mellitus
Research

Citer dette

@article{bd3b6f1227d8427e9673041eead0179a,
title = "Impaired TCA cycle flux in mitochondria in skeletal muscle from type 2 diabetic subjects: Marker or maker of the diabetic phenotype?",
abstract = "The diabetic phenotype is complex, requiring elucidation of key initiating defects. Recent research has shown that diabetic myotubes express a primary reduced tricarboxylic acid (TCA) cycle flux. A reduced TCA cycle flux has also been shown both in insulin resistant offspring of T2D patients and exercising T2D patients in vivo. This review will discuss the latest advances in the understanding of the molecular mechanisms regulating the TCA cycle with focus on possible underlying mechanism which could explain the impaired TCA flux in insulin resistant human skeletal muscle in type 2 diabetes. A reduced TCA is both a marker and a maker of the diabetic phenotype.",
author = "Michael Gaster and Nehlin, {Jan O} and Minet, {Ariane D}",
year = "2012",
doi = "10.3109/13813455.2012.656653",
language = "English",
volume = "118",
pages = "156--89",
journal = "Archives of Physiology and Biochemistry",
issn = "1381-3455",
publisher = "Taylor & Francis",
number = "3",

}

Impaired TCA cycle flux in mitochondria in skeletal muscle from type 2 diabetic subjects : Marker or maker of the diabetic phenotype? / Gaster, Michael; Nehlin, Jan O; Minet, Ariane D.

I: Archives of Physiology and Biochemistry, Bind 118, Nr. 3, 2012, s. 156-89.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

TY - JOUR

T1 - Impaired TCA cycle flux in mitochondria in skeletal muscle from type 2 diabetic subjects

T2 - Marker or maker of the diabetic phenotype?

AU - Gaster, Michael

AU - Nehlin, Jan O

AU - Minet, Ariane D

PY - 2012

Y1 - 2012

N2 - The diabetic phenotype is complex, requiring elucidation of key initiating defects. Recent research has shown that diabetic myotubes express a primary reduced tricarboxylic acid (TCA) cycle flux. A reduced TCA cycle flux has also been shown both in insulin resistant offspring of T2D patients and exercising T2D patients in vivo. This review will discuss the latest advances in the understanding of the molecular mechanisms regulating the TCA cycle with focus on possible underlying mechanism which could explain the impaired TCA flux in insulin resistant human skeletal muscle in type 2 diabetes. A reduced TCA is both a marker and a maker of the diabetic phenotype.

AB - The diabetic phenotype is complex, requiring elucidation of key initiating defects. Recent research has shown that diabetic myotubes express a primary reduced tricarboxylic acid (TCA) cycle flux. A reduced TCA cycle flux has also been shown both in insulin resistant offspring of T2D patients and exercising T2D patients in vivo. This review will discuss the latest advances in the understanding of the molecular mechanisms regulating the TCA cycle with focus on possible underlying mechanism which could explain the impaired TCA flux in insulin resistant human skeletal muscle in type 2 diabetes. A reduced TCA is both a marker and a maker of the diabetic phenotype.

U2 - 10.3109/13813455.2012.656653

DO - 10.3109/13813455.2012.656653

M3 - Journal article

VL - 118

SP - 156

EP - 189

JO - Archives of Physiology and Biochemistry

JF - Archives of Physiology and Biochemistry

SN - 1381-3455

IS - 3

ER -