title: Exercise training increases membrane bound form of tumor necrosis factor-alpha receptors with decreases in the secretion of soluble forms of receptors in rat adipocytes.
abstract: We examined the effects of exercise training (treadmill running over 9 weeks) on the ability of isolated adipocytes to secrete tumor necrosis factor-alpha (TNF-alpha) and type 1 soluble TNF receptor (sTNFR1) in vitro in Wistar rats. We also examined the effects of exercise training on the expression of membrane bound forms of type 1 TNF receptor (mTNFR1) in adipocyte crude membranes of the same rat subjects. Exercise training significantly increased the secretions of TNF-alpha from isolated adipocytes. Treatment with a cyclooxygenase inhibitor, either indomethacin (100 microM) or eicosatetraynoic acid (100 microM), significantly blocked the release of TNF-alpha from adipocytes in both exercise-trained rat group and sedentary control rat group, suggesting that some cyclooxygenase metabolite(s) acts as a ligand in TNF-alpha synthesis. Decreased amounts of TNF-alpha were found to be significantly greater in both exercise-trained rat group than in sedentary control rat group after incubation with inhibitors. Thus, the inhibitory effect of both indomethacin and eicosatetraynoic acid was significantly greater in adipocytes from exercise-trained rats. Both plasma sTNFR1 levels and adipocytes-derived sTNFR1 were found to be significantly less in the exercise-trained rat group. Western blot analysis revealed that exercise training remarkably increased the expressions of mTNFR1 in adipocyte crude membrane. Thus, exercise training enhanced the ability of isolated adipocytes to secrete TNF-alpha with reduced secretion of sTNFR1, and provoked the greater expressions of mTNFR1 in adipocyte crude membrane. These alterations may induce enhanced the autocrine effects of TNF-alpha within adipocytes in exercise-trained rats.
authors.affiliation: Department of Kinesiology, Graduate School of Science, Tokyo Metropolitan University, 1-1, Minami-ohsawa, Hachioji, 192-0397, Tokyo, Japan.
authors.forename: Yukihiko
authors.initials: Y
authors.lastname: Ito
authors.forename: Sachiko
authors.initials: S
authors.lastname: Nomura
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ueda
authors.forename: Takuya
authors.initials: T
authors.lastname: Sakurai
authors.forename: Takako
authors.initials: T
authors.lastname: Kizaki
authors.forename: Hideki
authors.initials: H
authors.lastname: Ohno
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Izawa
mesh_terms: D015117:5,8,11,14-Eicosatetraynoic Acid / Q000494:pharmacology; D017667:Adipocytes / Q000166:cytology / Q000378:metabolism*; D000818:Animals; D001835:Body Weight; D002462:Cell Membrane / Q000378:metabolism; D002478:Cells, Cultured; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D010805:Physical Conditioning, Animal; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D018124:Receptors, Tumor Necrosis Factor / Q000097:blood / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: D016861:Cyclooxygenase Inhibitors; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D015117:5,8,11,14-Eicosatetraynoic Acid; D007213:Indomethacin