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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3-5
pubmed:dateCreated
2008-5-26
pubmed:abstractText
Testosterone (T) is an important factor for determining body composition in males. Abdominal obesity is inversely correlated with serum T levels in men, leading to greater mortality. Pathologically hypogonadal men also have a significantly higher fat mass, which is reversed by T administration. However, the mechanism for such anti-obesity effect of androgen has not been well clarified. Androgen receptor (AR) null male mice revealed late-onset obesity. Male ARKO mice were euphagic compared to the wild-type male controls, but also less dynamic and less oxygen consuming. Transcript profiling indicated that male ARKO mice had lower transcripts for the thermogenetic uncoupling protein 1 (UCP1). We also found enhanced secretion of adiponectin, which is insulin-sensitizing, from adipose tissue in comparison to wild type, which might partly explain why the overall insulin sensitivity of male ARKO mice remained almost intact despite their apparent obesity. In addition, decreased lipolysis rather than increased lipid synthesis was observed, which might also account for the increased adiposity in male ARKO mice. The results revealed that AR plays important roles in male metabolism by affecting the energy balance, and is negative to both adiposity and insulin sensitivity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0960-0760
pubmed:author
pubmed:issnType
Print
pubmed:volume
109
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
254-7
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Androgens and metabolic syndrome: lessons from androgen receptor knock out (ARKO) mice.
pubmed:affiliation
Department of Medicine and Bioregulatory Science, Kyushu University, Maidashi 3-1-1, Fukuoka 812-8582, Japan. yanase@intmed3.med.kyushu-u.ac.jp
pubmed:publicationType
Journal Article