title: Tissue-specific expression of the uncoupling protein family in streptozotocin-induced diabetic rats.
abstract: The vulnerability of streptozotocin (STZ)-induced diabetic rats to cold stress has been established. One of the elements controlling body temperature is thermogenesis, in which uncoupling protein (UCP) is known to play an important role. We have examined UCP2 and UCP3 expressions in brown adipose tissue (BAT), white adipose tissue (WAT), and skeletal muscle (MSL) during the acute and chronic phases of STZ-induced diabetes in rats. The long-term effect and the effect of insulin treatment thereafter were also unexplored previously and are examined in this study. In the acute phase of diabetes (2.5 days after STZ injection), UCP2 gene expression in BAT, WAT, and MSL, and UCP3 expression in the muscle were significantly increased. In the chronic phase of diabetes (21 days after STZ injection), UCP2 and UCP3 expression in the MSL were restored to the control levels without insulin supplementation. UCP2 in BAT and WAT remained high in the chronic phase, whereas UCP3 expression in BAT and WAT, which did not change in the acute phase, was significantly decreased. Insulin supplementation restored UCP2 expression in BAT and WAT, but over-corrected UCP3 in WAT above the control and did not affect UCP3 expression in BAT. Insulin supplementation depressed UCP3 expression in the MSL below control. These results indicate that the effects of STZ-induced diabetes on UCPs gene expression are tissue-specific as well as dependent on the duration of diabetes.
authors.affiliation: Department of Internal Medicine I, School of Medicine, Oita Medical University, Oita, 879-5593, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Hidaka
authors.forename: H
authors.initials: H
authors.lastname: Yoshimatsu
authors.forename: T
authors.initials: T
authors.lastname: Kakuma
authors.forename: H
authors.initials: H
authors.lastname: Sakino
authors.forename: S
authors.initials: S
authors.lastname: Kondou
authors.forename: R
authors.initials: R
authors.lastname: Hanada
authors.forename: K
authors.initials: K
authors.lastname: Oka
authors.forename: Y
authors.initials: Y
authors.lastname: Teshima
authors.forename: M
authors.initials: M
authors.lastname: Kurokawa
authors.forename: T
authors.initials: T
authors.lastname: Sakata
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D002001:Adipose Tissue, Brown / Q000378:metabolism*; D000818:Animals; D001835:Body Weight; D002352:Carrier Proteins / Q000235:genetics*; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism*; D005786:Gene Expression Regulation / Q000187:drug effects; D007328:Insulin / Q000627:therapeutic use; D007473:Ion Channels; D008297:Male; D026901:Membrane Transport Proteins; D024101:Mitochondrial Proteins; D018482:Muscle, Skeletal / Q000378:metabolism*; D009928:Organ Specificity; D011506:Proteins / Q000235:genetics*; D051381:Rats; D017208:Rats, Wistar; D014475:Uncoupling Agents; D000071246:Uncoupling Protein 2; D000071247:Uncoupling Protein 3
chemical_list: D002352:Carrier Proteins; D007328:Insulin; D007473:Ion Channels; D026901:Membrane Transport Proteins; D024101:Mitochondrial Proteins; D011506:Proteins; C000604391:Ucp2 protein, rat; C000604394:Ucp3 protein, rat; D014475:Uncoupling Agents; D000071246:Uncoupling Protein 2; D000071247:Uncoupling Protein 3