[1]姜藻航,贺丹丹,夏梦圆,等.AdipoR2介导C2C12肌管细胞促进3T3-L1前体脂肪细胞的糖代谢能力[J].南京农业大学学报,2018,41(5):911-916.[doi:10.7685/jnau.201709012]
 JIANG Zaohang,HE Dandan,XIA Mengyuan,et al.Mediation of AdipoR2 in 3T3-L1 preadipocytes co-cultured with C2C12 myotubes for glucose absorption and consumption[J].Journal of Nanjing Agricultural University,2018,41(5):911-916.[doi:10.7685/jnau.201709012]
点击复制

AdipoR2介导C2C12肌管细胞促进3T3-L1前体脂肪细胞的糖代谢能力()
分享到:

《南京农业大学学报》[ISSN:1000-2030/CN:32-1148/S]

卷:
41卷
期数:
2018年5期
页码:
911-916
栏目:
出版日期:
2018-09-20

文章信息/Info

Title:
Mediation of AdipoR2 in 3T3-L1 preadipocytes co-cultured with C2C12 myotubes for glucose absorption and consumption
作者:
姜藻航 贺丹丹 夏梦圆 李振 陈杰
南京农业大学动物科技学院, 江苏 南京 210095
Author(s):
JIANG Zaohang HE Dandan XIA Mengyuan LI Zhen CHEN Jie
College of Animal Science and Technology, Nanjing Agricultural University, Nanjing 210095, China
关键词:
共培养脂联素受体23T3-L1前体脂肪细胞C2C12细胞
Keywords:
co-cultureAdipoR23T3-L1 preadipocyteC2C12 cells
分类号:
Q291
DOI:
10.7685/jnau.201709012
摘要:
[目的]本文旨在探究脂联素受体2(AdipoR2)在C2C12肌管细胞与3T3-L1前体脂肪细胞共培养体系中对3T3-L1前体脂肪细胞葡萄糖吸收与消耗能力的影响。[方法]利用siRNA干扰AdipoR2基因表达,同时利用Transwell细胞培养小室对这2种细胞进行了共培养并检验相关基因的表达水平和细胞葡萄糖消耗能力的变化。[结果]使用siRNA干扰AdipoR2基因的表达后,3T3-L1前体脂肪细胞的AdipoR2基因和葡萄糖转运蛋白基因Slc2a1Slc2a4表达水平显著下降,3T3-L1前体细胞每单位所消耗的葡萄糖量也显著下降。而在与C2C12细胞共培环境下,3T3-L1前体细胞中AdipoR2基因和葡萄糖转运蛋白Slc2a1、Slc2a4基因表达水平显著上调。同时,3T3-L1前体细胞单位消耗的葡萄糖量显著上升。进一步研究发现,AdipoR2能够有效调节3T3-L1前体脂肪细胞内葡萄糖转运蛋白基因的表达水平与葡萄糖的消耗能力。[结论]在C2C12肌管细胞共培体系中,AdipoR2能够加速3T3-L1前体脂肪细胞对葡萄糖的吸收。
Abstract:
[Objectives]This study was aimed to investigate the mediate capacity of AdipoR2 gene in 3T3-L1 preadipocytes co-cultured with C2C12 myotubes for the glucose absorption and consumption.[Methods]To testify the gene expression levels and glucose consumption in this co-culture system,we conducted siRNA to suppress the gene expression and Transwell inserts which allowing both of these two cells culturing in the same circumstance.[Results]Our data suggested that since the siRNA treatment,the 3T3-L1 preadipocytes significantly declined the expression of AdipoR2 gene,subsequently accompanied by the significant decrease of gene Slc2a1 and Slc2a4 expression. The glucose consumption test suggested that this capacity was in a lower degree compared to the control group as well. Additionally,in co-culture system AdipoR2 and glucose transport gene were higher significantly expressed resulting in the increment of the glucose content per protein unit. This way indicated that AdipoR2 gene in 3T3-L1 preadipocytes could regulate the glucose transport gene Slc2a1 and Slc2a4 expression and affect the glucose consumption ability.[Conclusions]In summary,to cope with the co-culture influence brought by C2C12 myotubes,AdipoR2 would like to significantly enhance the glucose consumption ability in 3T3-L1 preadipocytes.

参考文献/References:

[1] Joulia D,Bernardi H,Garandel V,et al. Mechanisms involved in the inhibition of myoblast proliferation and differentiation by myostatin[J]. Experimental Cell Research,2003,286(2):263-275.
[2] Sciorati C,Clementi E,Manfredi A A,et al. Fat deposition and accumulation in the damaged and inflamed skeletal muscle:cellular and molecular players[J]. Cellular and Molecular Life Sciences,2015,72(11):2135-2156.
[3] Buch A,Carmeli E,Boker L K,et al. Muscle function and fat content in relation to sarcopenia,obesity and frailty of old age:an overview[J]. Experimental Gerontology,2016,76:25-32.
[4] Yamauchi T,Kamon J,Ito Y,et al. Cloning of adiponectin receptors that mediate antidiabetic metabolic effects[J]. Nature,2003,423(6941):762-769.
[5] Kharroubi I,Rasschaert J,Eizirik D L,et al. Expression of adiponectin receptors in pancreatic beta cells[J]. Biochemical and Biophysical Research Communications,2003,312(4):1118-1122.
[6] Yamauchi T,Nio Y,Maki T,et al. Targeted disruption of AdipoR1 and AdipoR2 causes abrogation of adiponectin binding and metabolic actions[J]. Nature Medicine,2007,13(3):332-339.
[7] Wu M H,Huang S B,Lee G B. Microfluidic cell culture systems for drug research[J]. Lab Chip,2010,10(8):939-956.
[8] Androulakis I P. Systems engineering meets quantitative systems pharmacology:from low-level targets to engaging the host defenses[J]. Wiley Interdisciplinary Reviews Systems Biology and Medicine,2015,7(3):101-112.
[9] Tan X C,Chua K H,Ravishankar R M,et al. Monoterpenes:novel insights into their biological effects and roles on glucose uptake and lipid metabolism in 3T3-L1 adipocytes[J]. Food Chemistry,2016,196:242-250.
[10] Goers L,Freemont P,Polizzi K M. Co-culture systems and technologies:taking synthetic biology to the next level[J]. Journal of the Royal Society,Interface,2014,11(96):65-70. DOI:10.1098/rsif.2014.0065.
[11] Huang W C,Chang W T,Wu S J,et al. Phloretin and phlorizin promote lipolysis and inhibit inflammation in mouse 3T3-L1 cells and in macrophage-adipocyte co-cultures[J]. Molecular Nutrition & Food Research,2013,57(10):1803-1813.
[12] Tsuchida A,Yamauchi T,Ito Y,et al. Insulin/Foxo1 pathway regulates expression levels of adiponectin receptors and adiponectin sensitivity[J]. The Journal of Biological Chemistry,2004,279(29):30817-30822.
[13] Civitarese A E,Jenkinson C P,Richardson D,et al. Adiponectin receptors gene expression and insulin sensitivity in non-diabetic Mexican Americans with or without a family history of Type 2 diabetes[J]. Diabetologia,2004,47(5):816-820.
[14] Iwabu M,Yamauchi T,Okada-Iwabu M,et al. Adiponectin and AdipoR1 regulate PGC-1alpha and mitochondria by Ca(2+)and AMPK/SIRT1[J]. Nature,2010,464(7293):1313-1319.
[15] Bricker D K,Taylor E B,Schell J C,et al. A mitochondrial pyruvate carrier required for pyruvate uptake in yeast,Drosophila,and humans[J]. Science,2012,337(6090):96-100.
[16] Peters K E,Beilby J,Cadby G,et al. A comprehensive investigation of variants in genes encoding adiponectin(ADIPOQ)and its receptors(ADIPOR1/R2),and their association with serum adiponectin,type 2 diabetes,insulin resistance and the metabolic syndrome[J]. BMC Medical Genetics,2013,14:15.
[17] Pandurangan M,Jeong D,Amna T,et al. Co-culture of C2C12 and 3T3-L1 preadipocyte cells alters the gene expression of calpains,caspases and heat shock proteins[J]. In vitro Cellular & Developmental Biology Animal,2012,48(9):577-582.
[18] Ravikumar S,Muthuraman P. Cortisol effect on heat shock proteins in the C2C12 and 3T3-L1 cells[J]. In vitro Cellular & Developmental Biology Animal,2014,50(7):581-586.
[19] Tanaka T,Nakatani K,Morioka K,et al. Nitric oxide stimulates glucose transport through insulin-independent GLUT4 translocation in 3T3-L1 adipocytes[J]. European Journal of Endocrinology,2003,149(1):61-67.
[20] Canova N,Lincova D,Farghali H. Inconsistent role of nitric oxide on lipolysis in isolated rat adipocytes[J]. Physiological Research,2005,54(4):387-393.

备注/Memo

备注/Memo:
收稿日期:2017-9-5。
基金项目:国家科技支撑计划项目(2015BAD03B01)
作者简介:姜藻航,硕士研究生。
通信作者:陈杰,教授,研究方向为动物分子遗传与育种,E-mail:jiechen@njau.edu.cn。
更新日期/Last Update: 1900-01-01