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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004233naa a2200505 4500
001oai:DiVA.org:liu-102775
003SwePub
008131226s2013 | |||||||||||000 ||eng|
009oai:DiVA.org:hig-38202
009oai:prod.swepub.kib.ki.se:127845513
024a https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-1027752 URI
024a https://doi.org/10.1530/JOE-13-01892 DOI
024a https://urn.kb.se/resolve?urn=urn:nbn:se:hig:diva-382022 URI
024a http://kipublications.ki.se/Default.aspx?queryparsed=id:1278455132 URI
040 a (SwePub)liud (SwePub)higd (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Fransson, Liselotteu Karolinska Institutet4 aut
2451 0a beta-cell adaptation in a mouse model of glucocorticoid-induced metabolic syndrome
264 1b BioScientifica,c 2013
338 a print2 rdacarrier
500 a Funding Agencies|Diabetes Research and Wellness Foundation||Swedish Diabetes Foundation (Diabetesfonden)||Tore Nilsson Foundation||Swedish Society for Medical Research||KID (Karolinska Institutet)||
520 a Glucocorticoids (GCs) are stress hormones primarily responsible for mobilizing glucose to the circulation. Due to this effect, insulin resistance and glucose intolerance are concerns in patients with endogenous overproduction of GCs and in patients prescribed GC-based therapy. In addition, hypercortisolemic conditions share many characteristics with the metabolic syndrome. This study reports on a thorough characterization, in terms of glucose control and lipid handling, of a mouse model where corticosterone is given via the drinking water. C57BL/6J mice were treated with corticosterone (100 or 25 mu g/ml) or vehicle in their drinking water for 5 weeks after which they were subjected to insulin or glucose tolerance tests. GC-treated mice displayed increased food intake, body weight gain, and central fat deposit accumulations. In addition, the GC treatment led to dyslipidemia as well as accumulation of ectopic fat in the liver and skeletal muscle, having a substantial negative effect on insulin sensitivity. Also glucose intolerance and hypertension, both part of the metabolic syndrome, were evident in the GC-treated mice. However, the observed effects of corticosterone were reversed after drug removal. Furthermore, this study reveals insights into beta-cell adaptation to the GC-induced insulin resistance. Increased pancreatic islet volume due to cell proliferation, increased insulin secretion capacity, and increased islet chaperone expression were found in GC-treated animals. This model mimics the human metabolic syndrome. It could be a valuable model for studying the complex mechanisms behind the development of the metabolic syndrome and type 2 diabetes, as well as the multifaceted relations between GC excess and disease.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicin0 (SwePub)3022 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicine0 (SwePub)3022 hsv//eng
653 a glucocorticoid
653 a diabetes
653 a insulin secretion
653 a obesity
653 a islet cells
653 a MEDICINE
653 a MEDICIN
700a Franzén, Stephanieu Linköpings universitet,Avdelningen för läkemedelsforskning,Hälsouniversitetet,Linköpings universitet, Avdelningen för läkemedelsforskning4 aut0 (Swepub:liu)stefr34
700a Rosengren, Victoriau Karolinska Institutet4 aut
700a Wolbert, Petrau Soder Sjukhuset, Sweden4 aut
700a Sjöholm, Åkeu Soder Sjukhuset, Sweden4 aut0 (Swepub:hig)akesjm
700a Ortsater, Henriku Soder Sjukhuset, Sweden4 aut
710a Karolinska Institutetb Avdelningen för läkemedelsforskning4 org
773t Journal of Endocrinologyd : BioScientificag 219:3, s. 231-241q 219:3<231-241x 0022-0795x 1479-6805
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-102775
8564 8u https://doi.org/10.1530/JOE-13-0189
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:hig:diva-38202
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:127845513

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