title: Humoral regulation of resistin expression in 3T3-L1 and mouse adipose cells.
abstract: Resistin is a hormone secreted by adipocytes that acts on skeletal muscle myocytes, hepatocytes, and adipocytes themselves, reducing their sensitivity to insulin. In the present study, we investigated how the expression of resistin is affected by glucose and by mediators known to affect insulin sensitivity, including insulin, dexamethasone, tumor necrosis factor-alpha (TNF-alpha), epinephrine, and somatropin. We found that resistin expression in 3T3-L1 adipocytes was significantly upregulated by high glucose concentrations and was suppressed by insulin. Dexamethasone increased expression of both resistin mRNA and protein 2.5- to 3.5-fold in 3T3-L1 adipocytes and by approximately 70% in white adipose tissue from mice. In contrast, treatment with troglitazone, a thiazolidinedione antihyperglycemic agent, or TNF-alpha suppressed resistin expression by approximately 80%. Epinephrine and somatropin were both moderately inhibitory, reducing expression of both the transcript and the protein by 30-50% in 3T3-L1 adipocytes. Taken together, these data make it clear that resistin expression is regulated by a variety of hormones and that cytokines are related to glucose metabolism. Furthermore, they suggest that these factors affect insulin sensitivity and fat tissue mass in part by altering the expression and eventual secretion of resistin from adipose cells.
authors.affiliation: Department of Internal Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Shojima
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Sakoda
authors.forename: Takehide
authors.initials: T
authors.lastname: Ogihara
authors.forename: Midori
authors.initials: M
authors.lastname: Fujishiro
authors.forename: Hideki
authors.initials: H
authors.lastname: Katagiri
authors.forename: Motonobu
authors.initials: M
authors.lastname: Anai
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Onishi
authors.forename: Hiraku
authors.initials: H
authors.lastname: Ono
authors.forename: Kouichi
authors.initials: K
authors.lastname: Inukai
authors.forename: Miho
authors.initials: M
authors.lastname: Abe
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Fukushima
authors.forename: Masatoshi
authors.initials: M
authors.lastname: Kikuchi
authors.forename: Yoshitomo
authors.initials: Y
authors.lastname: Oka
authors.forename: Tomoichiro
authors.initials: T
authors.lastname: Asano
mesh_terms: D016475:3T3 Cells; D017667:Adipocytes / Q000378:metabolism*; D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D002839:Chromans / Q000494:pharmacology; D003907:Dexamethasone / Q000494:pharmacology; D004822:Epididymis; D004837:Epinephrine / Q000494:pharmacology; D015870:Gene Expression; D005938:Glucocorticoids / Q000494:pharmacology; D005947:Glucose / Q000494:pharmacology*; D006729:Hormones, Ectopic / Q000235:genetics*; D019382:Human Growth Hormone / Q000494:pharmacology; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007328:Insulin / Q000494:pharmacology*; D036341:Intercellular Signaling Peptides and Proteins; D008297:Male; D051379:Mice; D020932:Nerve Growth Factor; D011506:Proteins; D012333:RNA, Messenger / Q000032:analysis; D052243:Resistin; D013844:Thiazoles / Q000494:pharmacology; D045162:Thiazolidinediones; D000077288:Troglitazone; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D002839:Chromans; D005938:Glucocorticoids; D006729:Hormones, Ectopic; D007004:Hypoglycemic Agents; D007328:Insulin; D036341:Intercellular Signaling Peptides and Proteins; D011506:Proteins; C486574:RETNLB protein, human; D012333:RNA, Messenger; D052243:Resistin; C499623:Retn protein, mouse; C413576:Retnla protein, mouse; D013844:Thiazoles; D045162:Thiazolidinediones; D014409:Tumor Necrosis Factor-alpha; D019382:Human Growth Hormone; D003907:Dexamethasone; D020932:Nerve Growth Factor; D000077288:Troglitazone; D005947:Glucose; D004837:Epinephrine