title: CTRP3 modulates the expression and secretion of adipokines in 3T3-L1 adipocytes.
abstract: The objective of this study was to investigate the impact of C1q/TNF related protein 3 (CTRP3), a novel adipokine, on the expression and secretion of adiponectin, leptin, visfatin, and apelin in 3T3-L1 adipocytes. The effect of insulin resistance on the impact was also investigated. 3T3-L1 adipocytes were treated with different concentrations (0, 10, 50, 250, 1250 ng/mL) CTRP3 for 12 h, and with 250 ng/mL CTRP3 for different times (0, 6, 12, 24, 48 h). The expression of adipokines between normal and insulin resistant adipocytes, as well as between the adipocytes pre-treated with and without Compound C were compared. The secretion and gene expression of the adipokines were detected by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (RT-PCR), respectively. The relative expression of AMPK (thr172) was detected by western blot analysis. With the increase in CTRP3 concentration or the duration of the treatment, the secretion of adiponectin, leptin, visfatin and apelin were all increased accordingly, which was significant under the treatment with 250 ng/mL and 1250 ng/mL CTRP3 for 12 h as well as 250 ng/mL CTRP3 for 12 h, 24 h and 48 h. Gene expression showed a similar trend. The secretion and gene expression of adipokines in insulin resistant adipocytes were all decreased significantly in comparison with that of normal adipocytes. The secretion secretion and gene expression of adiponectin, and the relative expression of AMPK (thr172) in adipocytes pre-treated with Compound C were decreased significantly in comparison with that in adipocytes without Compound C pretreatment. Thus, CTRP3 increased the expression and secretion of adiponectin, leptin, visfatin, and apelin in 3T3-L1 adipocytes, while insulin resistance inhibited the effects. CTRP3 up-regulated the expression of adiponectin in 3T3-L1 adipocytes through AMPK signaling pathway.
authors.affiliation: Department of Endocrinology, Zhongnan Hospital, Wuhan University, Wuhan 430071, China.
authors.forename: Xin
authors.initials: X
authors.lastname: Li
authors.forename: Li
authors.initials: L
authors.lastname: Jiang
authors.forename: Miao
authors.initials: M
authors.lastname: Yang
authors.forename: Yu-wen
authors.initials: YW
authors.lastname: Wu
authors.forename: Su-xin
authors.initials: SX
authors.lastname: Sun
authors.forename: Jia-zhong
authors.initials: JZ
authors.lastname: Sun
mesh_terms: D041721:3T3-L1 Cells; D055372:AMP-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D052438:Adipocytes, White / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D054392:Adipokines / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D000073861:Apelin; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism; D007333:Insulin Resistance; D036341:Intercellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism*; D007700:Kinetics; D051379:Mice; D054409:Nicotinamide Phosphoribosyltransferase / Q000235:genetics / Q000378:metabolism*; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D011720:Pyrazoles / Q000494:pharmacology; D011743:Pyrimidines / Q000494:pharmacology; D011994:Recombinant Proteins / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D054392:Adipokines; D000073861:Apelin; C402826:Apln protein, mouse; C428135:CORS26 protein, mouse; D016207:Cytokines; D036341:Intercellular Signaling Peptides and Proteins; D047428:Protein Kinase Inhibitors; D011720:Pyrazoles; D011743:Pyrimidines; D011994:Recombinant Proteins; C516138:dorsomorphin; D054409:Nicotinamide Phosphoribosyltransferase; C495867:nicotinamide phosphoribosyltransferase, mouse; D055372:AMP-Activated Protein Kinases; D005947:Glucose