Humoral regulation of resistin expression in 3T3-L1 and mouse adipose cells.
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.
Shojima
Nobuhiro
N
Department of Internal Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
Sakoda
Hideyuki
H
Ogihara
Takehide
T
Fujishiro
Midori
M
Katagiri
Hideki
H
Anai
Motonobu
M
Onishi
Yukiko
Y
Ono
Hiraku
H
Inukai
Kouichi
K
Abe
Miho
M
Fukushima
Yasushi
Y
Kikuchi
Masatoshi
M
Oka
Yoshitomo
Y
Asano
Tomoichiro
T
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
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