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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2003-5-21
pubmed:abstractText
To examine whether the effects of high-fat feeding on glycogen synthase (GS) activity and mRNA levels differ between diabetes-prone (C57BL/6J) and diabetes-resistant mice (NMRI), we measured GS activity and mRNA levels in muscle from C57BL/6J and NMRI mice fed a high-fat or normal chow diet for 3, 6, and 15 months. As compared with chow feeding, fat feeding increased plasma insulin levels in C57BL/6J mice at 15 months (464 +/- 29 v 267 +/- 47 pmol/L, P =.005), which was associated with elevated plasma glucose levels at 15 months (5.3 +/- 0.3 v 3.8 +/- 0.2 mmol/L, P =.001). Fat feeding increased plasma insulin levels also in NMRI mice at 15 months (705 +/- 145 v 275 +/- 64 pmol/L, P =.01) without, however, a rise of plasma glucose levels. In parallel with increased insulin levels, decreased muscle GS fractional velocity (FV) was observed at 6 (49.0% +/- 2.6% v 69.1% +/- 7.3%, P =.04) and 15 (45.8% +/- 1.8% v 53.4% +/- 1.6 %, P <.01) months but not at 3 months in the fat-fed C57BL/6J mice. Similarly, there was a significant decrease in GS fractional activity at 3 (57.9% +/- 4.3% v 70.4% +/- 2.6 %, P <.03) and 15 (47.3% +/- 2.4% v 56.4% +/- 2.1%, P =.02) but not at 6 months in the fat-fed NMRI mice. The decrease in GS activity was not associated with changes in mRNA levels at any time points. We conclude that (1) fat feeding results in similar elevation of plasma insulin levels and impairs GS activity in C57BL/6J and NMRI mice, and (2) the changes in GS activity do not involve effects on gene expression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0026-0495
pubmed:author
pubmed:copyrightInfo
Copyright 2003 Elsevier Inc. All rights reserved.
pubmed:issnType
Print
pubmed:volume
52
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
535-9
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Fat feeding impairs glycogen synthase activity in mice without effects on its gene expression.
pubmed:affiliation
Wallenberg Laboratory, Department of Endocrinology, University of Lund, Malmo, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't