Knockdown of LYRM1 Rescues Insulin Resistance and Mitochondrial Dysfunction Induced by FCCP in 3T3-L1 Adipocytes

Cell Biochemistry and Biophysics

Volumn 70, Issue 1, 2014, Pages 667-675

  Zhang, Min ^a   Qin, Zhen Ying ^b   Dai, Yong mei ^a   Wang, Yu Mei ^c   Zhu, Guan zhong ^d   Zhao, Ya Ping ^e   Ji, Chen Bo ^a   Zhu, Jin Gai ^a   Shi, Chun Mei ^d   Qiu, Jie ^a   Cao, Xin Guo ^a   Guo, Xi Rong ^d  

^a WOMEN S HOSPITAL OF NANJING MEDICAL UNIVERSITY   (China)

^b THE FIRST AFFILIATED HOSPITAL OF NANJING MEDICAL UNIVERSITY   (China)

^c Huai'an Maternal and Child Health Care Center   (China)

^d NANJING MEDICAL UNIVERSITY   (China)

^e The 82th Hospital of the People's Liberation Army   (China)

Author keywords

3T3 L1 adipocyte; FCCP; Insulin resistance; LYRM1; Mitochondrial dysfunction

Indexed keywords

ADENOSINE TRIPHOSPHATE; APOPTOSIS REGULATORY PROTEIN; CARBONYL CYANIDE 4 (TRIFLUOROMETHOXY)PHENYLHYDRAZONE; GLUCOSE; GLUCOSE TRANSPORTER 4; INSULIN; LYR MOTIF CONTAINING 1 PROTEIN, MOUSE; PROTON IONOPHORE; REACTIVE OXYGEN METABOLITE;

3T3 CELL LINE; ADIPOCYTE; ANIMAL; BIOSYNTHESIS; CYTOLOGY; DEFICIENCY; DRUG EFFECTS; GENE SILENCING; GENETICS; INSULIN RESISTANCE; METABOLISM; MITOCHONDRIAL MEMBRANE POTENTIAL; MITOCHONDRION; MOUSE; PHOSPHORYLATION; PROTEIN TRANSPORT; SIGNAL TRANSDUCTION;

3T3-L1 CELLS; ADENOSINE TRIPHOSPHATE; ADIPOCYTES; ANIMALS; APOPTOSIS REGULATORY PROTEINS; CARBONYL CYANIDE P-TRIFLUOROMETHOXYPHENYLHYDRAZONE; GENE KNOCKDOWN TECHNIQUES; GLUCOSE; GLUCOSE TRANSPORTER TYPE 4; INSULIN; INSULIN RESISTANCE; MEMBRANE POTENTIAL, MITOCHONDRIAL; MICE; MITOCHONDRIA; PHOSPHORYLATION; PROTEIN TRANSPORT; PROTON IONOPHORES; REACTIVE OXYGEN SPECIES; SIGNAL TRANSDUCTION;

EID: 84906243977     PISSN: 10859195     EISSN: None     Source Type: Journal    
DOI: 10.1007/s12013-014-9971-y     Document Type: Article

References (34)

1. Jeffery, R. W., & Sherwood, N. E. (2008). Is the obesity epidemic exaggerated? No. BMJ, 336(7638), 245.
2. Walley, A. J., Asher, J. E., & Froguel, P. (2009). The genetic contribution to non-syndromic human obesity. Nature Reviews Genetics, 10(7), 431-442.
3. Zimmet, P., Alberti, K. G., & Shaw, J. (2001). Global and societal implications of the diabetes epidemic. Nature, 414(6865), 782-787.
4. Stumvoll, M., Goldstein, B. J., & van Haeften, T. W. (2008). Type 2 diabetes: Pathogenesis and treatment. Lancet, 371(9631), 2153-2156.
5. Qiu, J., et al. (2009). LYRM1, a novel gene promotes proliferation and inhibits apoptosis of preadipocytes. European Journal of Endocrinology, 160(2), 177-184.
6. Qiu, J., et al. (2007). Identification of differentially expressed genes in omental adipose tissues of obese patients by suppression subtractive hybridization. Biochemical and Biophysical Research Communications, 352(2), 469-478.
7. Cao, X. G., et al. (2010). Overexpression of LYRM1 induces mitochondrial impairment in 3T3-L1 adipocytes. Molecular Genetics and Metabolism, 101(4), 395-399.
8. Zhu, G. Z., et al. (2012). Effects of Lyrm1 knockdown on mitochondrial function in 3 T3-L1 murine adipocytes. Journal of Bioenergetics and Biomembranes, 44(1), 225-232.
9. Zhang, M., et al. (2012). Regulation of LYRM1 gene expression by free fatty acids, adipokines, and rosiglitazone in 3T3-L1 adipocytes. Experimental Diabetes Research, 2012, 820989.
10. Qin, Z. Y., et al. (2012). Alpha-Lipoic acid ameliorates impaired glucose uptake in LYRM1 overexpressing 3T3-L1 adipocytes through the IRS-1/Akt signaling pathway. Journal of Bioenergetics and Biomembranes, 44(5), 579-586.
11. Gunter, T. E., & Pfeiffer, D. R. (1990). Mechanisms by which mitochondria transport calcium. American Journal of Physiology, 258(5 Pt 1), C755-C786.
12. Dispersyn, G., et al. (1999). Bcl-2 protects against FCCP-induced apoptosis and mitochondrial membrane potential depolarization in PC12 cells. Biochimica et Biophysica Acta, 1428(2-3), 357-371.
13. Terada, H. (1990). Uncouplers of oxidative phosphorylation. Environmental Health Perspectives, 87, 213-218.
14. Chen, C., & Okayama, H. (1987). High-efficiency transformation of mammalian cells by plasmid DNA. Molecular and Cellular Biology, 7(8), 2745-2752.
15. Tejerina, S., et al. (2009). Mild mitochondrial uncoupling induces 3T3-L1 adipocyte de-differentiation by a PPARgamma-independent mechanism, whereas TNFalpha-induced de-differentiation is PPARgamma dependent. Journal of Cell Science, 122(Pt 1), 145-155.
16. Ceddia, R. B., et al. (2005). Globular adiponectin increases GLUT4 translocation and glucose uptake but reduces glycogen synthesis in rat skeletal muscle cells. Diabetologia, 48(1), 132-139.
17. Maxwell, D. P., Wang, Y., & McIntosh, L. (1999). The alternative oxidase lowers mitochondrial reactive oxygen production in plant cells. Proceedings of the National Academy of Sciences, USA, 96(14), 8271-8276.
18. Brown, G. C. (1992). Control of respiration and ATP synthesis in mammalian mitochondria and cells. Biochemical Journal, 284(Pt 1), 1-13.
19. Bonnard, C., et al. (2008). Mitochondrial dysfunction results from oxidative stress in the skeletal muscle of diet-induced insulin-resistant mice. The Journal of Clinical Investigation, 118(2), 789-800.
20. Kanzaki, M. (2006). Insulin receptor signals regulating GLUT4 translocation and actin dynamics. Endocrine Journal, 53(3), 267-293.
21. Bryant, N. J., Govers, R., & James, D. E. (2002). Regulated transport of the glucose transporter GLUT4. Nature Reviews Molecular Cell Biology, 3(4), 267-277.
22. Fact sheets from the Surgeon General's Call to. (2002). Action to prevent and decrease overweight and obesity. West Virginia Medical Journal, 98(6), 234-243.
23. Lewis, S., et al. (2010). "I don't eat a hamburger and large chips every day!" A qualitative study of the impact of public health messages about obesity on obese adults. BMC Public Health, 10, 309.
24. Giovannone, B., et al. (2000). Insulin receptor substrate (IRS) transduction system: Distinct and overlapping signaling potential. Diabetes/Metabolism Research and Reviews, 16(6), 434-441.
25. Shibata, M., et al. (2010). Paraquat-induced oxidative stress represses phosphatidylinositol 3-kinase activities leading to impaired glucose uptake in 3T3-L1 adipocytes. Journal of Biological Chemistry, 285(27), 20915-20925.
26. Bashan, N., et al. (2009). Positive and negative regulation of insulin signaling by reactive oxygen and nitrogen species. Physiological Reviews, 89(1), 27-71.
27. Houstis, N., Rosen, E. D., & Lander, E. S. (2006). Reactive oxygen species have a causal role in multiple forms of insulin resistance. Nature, 440(7086), 944-948.
28. Kou, C., et al. (2011). Over-expression of LYRM1 inhibits glucose transport in rat skeletal muscles via attenuated phosphorylation of PI3 K (p85) and Akt. Molecular and Cellular Biochemistry, 348(1-2), 149-154.
29. Kim, T., et al. (2009). Knockdown of JNK rescues 3T3-L1 adipocytes from insulin resistance induced by mitochondrial dysfunction. Biochemical and Biophysical Research Communications, 378(4), 772-776.
30. Ungvari, Z., et al. (2007). Increased mitochondrial H2O2 production promotes endothelial NF-kappaB activation in aged rat arteries. American Journal of Physiology Heart and Circulatory Physiology, 293(1), H37-H47.
31. Brennan, J. P., et al. (2006). Mitochondrial uncoupling, with low concentration FCCP, induces ROS-dependent cardioprotection independent of KATP channel activation. Cardiovascular Research, 72(2), 313-321.
32. Saotome, M., et al. (2005). Mitochondrial membrane potential modulates regulation of mitochondrial Ca2+ in rat ventricular myocytes. American Journal of Physiology Heart and Circulatory Physiology, 288(4), H1820-H1828.
33. Boden, G. (2011). Obesity, insulin resistance and free fatty acids. Current opinion in Endocrinology, Diabetes, and Obesity, 18(2), 139-143.
34. Kim, J. A., Wei, Y., & Sowers, J. R. (2008). Role of mitochondrial dysfunction in insulin resistance. Circulation Research, 102(4), 401-414.