Source:http://linkedlifedata.com/resource/pubmed/id/18006329
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
|
pubmed:dateCreated |
2007-12-6
|
pubmed:abstractText |
Thyroid hormones act on several aspects of metabolic and energy homeostasis influencing body weight, thermogenesis, and lipolysis in adipose tissue. Adipocytokines are biologically active substances produced by adipocyte with different physiological functions. These substances have multiple effects on several tissues acting on the intermediate and energy metabolism. For these reasons, attention has recently been focused on the possible relationship between adipocytokines, thyroid status, and thyroid dysfunction. Leptin, a signal of satiety to the brain and regulator of insulin and glucose metabolism, reflects the amount of fat storage and is considered as a pro-inflammatory adipocytokine. Adiponectin is inversely related to the degree of adiposity, increases insulin sensitivity, and may have antiatherogenic and anti-inflammatory properties. Resistin impairs glucose homeostasis and insulin action in mice but not in humans. Resistin might be considered a pro-inflammatory adipocytokine and participate in obesity-associated inflammation. Several reports indicate that leptin regulates thyroid function at hypothalamic-hypophyseal level and, conversely, thyroid hormones might control leptin metabolism at least in some animals studies. Both adiponectin and thyroid hormones share some physiological actions as reduction of body fat by increasing thermogenesis and lipid oxidation. Resistin also seems to be regulated by thyroid hormones, at least in rats. Thyroid dysfunction does not significantly affect serum leptin concentrations. Serum levels of adiponectin are no influenced by thyroid hypofunction; however, hyperthyroidism is associated with normal or elevated adiponectin levels. Finally, discordant results in resistin levels in thyroid dysfunction have been reported in humans.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Nov
|
pubmed:issn |
1096-0023
|
pubmed:author | |
pubmed:issnType |
Electronic
|
pubmed:volume |
40
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
61-70
|
pubmed:dateRevised |
2011-11-17
|
pubmed:meshHeading |
pubmed-meshheading:18006329-Adipokines,
pubmed-meshheading:18006329-Adiposity,
pubmed-meshheading:18006329-Animals,
pubmed-meshheading:18006329-Glucose,
pubmed-meshheading:18006329-Humans,
pubmed-meshheading:18006329-Hypothalamo-Hypophyseal System,
pubmed-meshheading:18006329-Insulin,
pubmed-meshheading:18006329-Mice,
pubmed-meshheading:18006329-Thyroid Diseases,
pubmed-meshheading:18006329-Thyroid Hormones
|
pubmed:year |
2007
|
pubmed:articleTitle |
Influence of thyroid dysfunction on serum concentrations of adipocytokines.
|
pubmed:affiliation |
Department of Endocrinology, Hospital General, 40002 Segovia, Spain. piglesias@hgse.sacyl.es
|
pubmed:publicationType |
Journal Article,
Review
|