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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2004-8-27
pubmed:abstractText
Interleukin-6 (IL-6) could be a possible mediator of insulin resistance. We investigated whether IL-6 could inhibit insulin signaling in human skeletal myotubes and whether suppressor of cytokine signaling 3 (SOCS-3) could be related to insulin resistance in vivo in humans. IL-6 inhibited insulin signaling and induced SOCS-3 expression in differentiated myotubes. SOCS-3 mRNA levels were significantly increased in the skeletal muscle of type 2 diabetic patients compared with control subjects and correlated with reduced insulin-stimulated glucose uptake. In contrast, SOCS-3 mRNA levels were reduced in muscle of obese nondiabetic subjects compared with type 2 diabetic patients, despite similar circulating concentrations of IL-6. Increased SOCS-3 mRNA levels in diabetes were not attributable to hyperglycemia, as type 1 diabetic patients had normal SOCS-3 mRNA expression in muscle. However, the combination of high glucose and IL-6 levels in type 2 diabetic patients may induce SOCS-3 expression, as has been seen in human muscle cells. In subcutaneous adipose tissue, SOCS-3 mRNA levels were increased in obese individuals and strongly correlated with IL-6 expression, supporting a paracrine effect of IL-6 on SOCS-3 expression in fat. Taken together, our results showed that SOCS-3 expression in human skeletal muscle in vivo is not related to insulin resistance in the presence of elevated IL-6 concentrations and suggest that cytokine action could differ in type 2 diabetic patients and nondiabetic obese subjects.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
53
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2232-41
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:15331532-Adipose Tissue, pubmed-meshheading:15331532-Adult, pubmed-meshheading:15331532-Cells, Cultured, pubmed-meshheading:15331532-Diabetes Mellitus, pubmed-meshheading:15331532-Diabetes Mellitus, Type 2, pubmed-meshheading:15331532-Female, pubmed-meshheading:15331532-Gene Expression, pubmed-meshheading:15331532-Humans, pubmed-meshheading:15331532-Hyperglycemia, pubmed-meshheading:15331532-Insulin, pubmed-meshheading:15331532-Insulin Resistance, pubmed-meshheading:15331532-Interleukin-6, pubmed-meshheading:15331532-Male, pubmed-meshheading:15331532-Middle Aged, pubmed-meshheading:15331532-Muscle, Skeletal, pubmed-meshheading:15331532-Muscle Fibers, Skeletal, pubmed-meshheading:15331532-Obesity, pubmed-meshheading:15331532-RNA, Messenger, pubmed-meshheading:15331532-Repressor Proteins, pubmed-meshheading:15331532-Signal Transduction, pubmed-meshheading:15331532-Suppressor of Cytokine Signaling Proteins, pubmed-meshheading:15331532-Transcription Factors
pubmed:year
2004
pubmed:articleTitle
Suppressor of cytokine signaling 3 expression and insulin resistance in skeletal muscle of obese and type 2 diabetic patients.
pubmed:affiliation
INSERM U449/INRA U1235, Faculté de Médecine René Laennec, Rue G. Paradin, F-69372 Lyon, Cedex 08, France. jennifer.rieusset@univ-lyon1.fr
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't