Roles of α-linolenic acid on IGF-I secretion and GH/IGF system gene expression in porcine primary hepatocytes.
The main purposes of this study were to investigate the effects of α-linolenic acid (ALA) on the insulin-like growth factor (IGF) system of porcine primary hepatocytes with or without growth hormone (GH) or insulin and the potential role of peroxisome proliferator-activated receptor α and -γ (PPARα/γ) pathway. We found that 1 μM ALA increased IGF-I secretion from hepatocytes at 48 and 72 h. Expression of hepatocytes IGF-I, IGF-II, GH receptor (GHR), insulin receptor (IR), IGF-binding protein 3 (IGFBP3), and IGFBP4 mRNAs was up-regulated by ALA treatment. GH (15 nM) alone or co-treated with ALA increased hepatocytes IGF-I secretion and the expression of GHR and IGFBP1 mRNAs, but down-regulated IGFBP5 mRNA compared with appropriate control across ALA. GH also enhanced the ALA-induced increase in the transcript levels of IGF-II and GHR, but tended to attenuate that of IGFBP4. Insulin (1 μM) alone or co-treated with ALA improved IGF-I secretion and the expression of IGFBP3 mRNA, but decreased IGFBP1 mRNA versus appropriate control across ALA. Insulin also up-regulated the expression of GHR, IR, IGFBP3, and IGFBP4 mRNAs, and tended to prevent the transcript levels of IGF-I and IGFBP4 improved by ALA. Both PPARγ agonist rosiglitazone and its antagonist GW9662 could elevated the IGF-I secretion in dose-dependent manner but they had no interaction with ALA. However, GW7647, a PPARα agonist, increased IGF-I secretion dose-dependently, but the antagonist GW6471 was without effect. Moreover, GW6471 prevented the IGF-I promoting effect of ALA. This suggests that the IGF-I promoting effect of ALA may be mediated by the PPARα pathway.
College of Animal Science, South China Agricultural University, No. 483 of Wushan Avenue, Tianhe District, Guangzhou, 510640, People's Republic of China.
Xin-Ling
XL
Fang
Gang
G
Shu
Zhi-Qi
ZQ
Zhang
Song-Bo
SB
Wang
Xiao-Tong
XT
Zhu
Ping
P
Gao
Qian-Yun
QY
Xi
Yong-Liang
YL
Zhang
Qing-Yan
QY
Jiang
D000818:Animals; D002087:Butyrates / Q000494:pharmacology; D002478:Cells, Cultured; D005786:Gene Expression Regulation / Q000187:drug effects*; D013006:Growth Hormone / Q000008:administration & dosage / Q000235:genetics* / Q000378:metabolism / Q000494:pharmacology; D022781:Hepatocytes / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000008:administration & dosage / Q000494:pharmacology; D007334:Insulin-Like Growth Factor I / Q000235:genetics / Q000378:metabolism*; D008024:Ligands; D047495:PPAR gamma / Q000378:metabolism; D010671:Phenylurea Compounds / Q000494:pharmacology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D034421:Sus scrofa / Q000235:genetics*; D017962:alpha-Linolenic Acid / Q000008:administration & dosage / Q000494:pharmacology*
D002087:Butyrates; C453899:GW 7647; D007328:Insulin; D008024:Ligands; D047495:PPAR gamma; D010671:Phenylurea Compounds; D012333:RNA, Messenger; D017962:alpha-Linolenic Acid; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone