Source:http://linkedlifedata.com/resource/pubmed/id/21249616
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2011-3-31
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pubmed:abstractText |
Local activation of glucocorticoids in insulin target tissues by the enzyme 11?-hydroxysteroid dehydrogenase type 1 (11?HSD1) has been implicated in the etiology of the metabolic syndrome. In obesity, adipose tissue 11?HSD1 is upregulated, leading to the generation of higher tissue levels of cortisol, which may increase insulin resistance. However, skeletal muscle is the predominant site of insulin-mediated glucose disposal, which is known to be reduced in obesity. We aimed to determine if there is any relationship between skeletal muscle 11?HSD1 and markers of central adiposity and insulin resistance in nondiabetic subjects. 20 nondiabetic volunteers (8 males and 12 females, mean age 55 ± 13 years, body mass index 21.5-47.6, mean 30.4 ± 1.6 kg/m (2)) underwent a single fasting blood sample followed by a muscle biopsy of vastus lateralis under local anesthetic. Fasting glucose, insulin and adiponectin were measured in serum. Skeletal muscle 11?HSD1 oxoreductase activity was determined by measuring the conversion of radiolabelled (3)H-cortisone to cortisol by thin layer chromatography. When subjects were categorised according to abdominal obesity (waist circumference ? 102 cm in men, ? 88 cm in women), there was no difference between the groups in skeletal muscle 11?HSD1 activity. There was no correlation between body mass index or waist circumference and 11?HSD1 activity or between HOMA and 11?HSD1 activity. Skeletal muscle 11?HSD1 oxoreductase activity is not altered in nondiabetic subjects with central obesity-associated insulin resistance. It is therefore unlikely that the in vivo insulin resistance observed in skeletal muscle of centrally obese subjects is mediated by alterations in 11?HSD1.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1439-4286
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pubmed:author | |
pubmed:copyrightInfo |
© Georg Thieme Verlag KG Stuttgart · New York.
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pubmed:issnType |
Electronic
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pubmed:volume |
43
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
257-60
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:21249616-11-beta-Hydroxysteroid Dehydrogenase Type 1,
pubmed-meshheading:21249616-Adult,
pubmed-meshheading:21249616-Aged,
pubmed-meshheading:21249616-Body Mass Index,
pubmed-meshheading:21249616-Female,
pubmed-meshheading:21249616-Glucose,
pubmed-meshheading:21249616-Humans,
pubmed-meshheading:21249616-Insulin,
pubmed-meshheading:21249616-Insulin Resistance,
pubmed-meshheading:21249616-Male,
pubmed-meshheading:21249616-Middle Aged,
pubmed-meshheading:21249616-Muscle, Skeletal,
pubmed-meshheading:21249616-Obesity, Abdominal
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pubmed:year |
2011
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pubmed:articleTitle |
Skeletal muscle 11?HSD1 activity of nondiabetic subjects is unaltered in central obesity-associated insulin resistance.
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pubmed:affiliation |
Department of Endocrinology, St Vincent's Hospital, Fitzroy, Victoria, Australia. winder@medstv.unimelb.edu.au
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pubmed:publicationType |
Journal Article,
Clinical Trial,
Research Support, Non-U.S. Gov't
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