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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003491naa a2200397 4500
001oai:DiVA.org:umu-19407
003SwePub
008090305s2008 | |||||||||||000 ||eng|
009oai:DiVA.org:uu-211258
024a https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-194072 URI
024a https://doi.org/10.1016/j.abb.2008.02.0342 DOI
024a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2112582 URI
040 a (SwePub)umud (SwePub)uu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Burén, Jonasu Umeå universitet,Medicin4 aut0 (Swepub:umu)jobu0003
2451 0a Insulin action and signalling in fat and muscle from dexamethasone-treated rats
264 1b Elsevier BV,c 2008
338 a print2 rdacarrier
520 a Glucocorticoids initiate whole body insulin resistance and the aim of the present study was to investigate effects of dexamethasone on protein expression and insulin signalling in muscle and fat tissue. Rats were injected with dexamethasone (1mg/kg/day, i.p.) or placebo for 11 days before insulin sensitivity was evaluated in vitro in soleus and epitrochlearis muscles and in isolated epididymal adipocytes. Dexamethasone treatment reduced insulin-stimulated glucose uptake and glycogen synthesis by 30-70% in epitrochlearis and soleus, and insulin-stimulated glucose uptake by approximately 40% in adipocytes. 8-bromo-cAMP-stimulated lipolysis was approximately 2-fold higher in adipocytes from dexamethasone-treated rats and insulin was less effective to inhibit cAMP-stimulated lipolysis. A main finding was that dexamethasone decreased expression of PKB and insulin-stimulated Ser(473) and Thr(308) phosphorylation in both muscles and adipocytes. Expression of GSK-3 was not influenced by dexamethasone treatment in muscles or adipocytes and insulin-stimulated GSK-3beta Ser(9) phosphorylation was reduced in muscles only. A novel finding was that glycogen synthase (GS) Ser(7) phosphorylation was higher in both muscles from dexamethasone-treated rats. GS expression decreased (by 50%) in adipocytes only. Basal and insulin-stimulated GS Ser(641) and GS Ser(645,649,653,657) phosphorylation was elevated in epitrochlearis and soleus muscles and GS fractional activity was reduced correspondingly. In conclusion, dexamethasone treatment (1) decreases PKB expression and insulin-stimulated phosphorylation in both muscles and adipocytes, and (2) increases GS phosphorylation (reduces GS fractional activity) in muscles and decreases GS expression in adipocytes. We suggest PKB and GS as major targets for dexamethasone-induced insulin resistance.
653 a Lipolysis
653 a Glycerol
653 a cAMP
653 a Glucocorticoids
653 a Phosphorylation
700a Lai, Y C4 aut
700a Lundgren, Magdalenau Umeå universitet,Medicin4 aut
700a Eriksson, Jan Wu Umeå universitet,Medicin,Department of Public Health and Clinical Medicine, Umeå University Hospital, Umeå, Sweden4 aut0 (Swepub:uu)janer909
700a Jensen, J4 aut
710a Umeå universitetb Medicin4 org
773t Archives of Biochemistry and Biophysicsd : Elsevier BVg 474:1, s. 91-101q 474:1<91-101x 0003-9861x 1096-0384
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-19407
8564 8u https://doi.org/10.1016/j.abb.2008.02.034
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-211258

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