Abstract OBJECTIVE: To study the effect of a new obesity-related gene NYGGF4 on the insulin sensitivity and secretory function of adipocytes. METHODS: 3T3-L1 preadipocytes transfected with either an empty expression vector (pcDNA3.1; control group) or an NYGGF4 expression vector (NYGGF4-pcDNA3.1) were cultured in vitro and differentiated into the matured adipocytes with the standard insulin plus dexamethasone plus 3-isobutyl-methylxanthine (MDI) induction cocktail. 2-deoxy-D-［3H］ glucose uptake was determined by liquid scintillation counting. Western blot was performed to detect the protein content and translocation of glucose transporter 4 (GLUT4). The supernatant concentrations of TNF-α, IL-6, adiponectin and resistin were measured using ELISA. RESULTS: NYGGF4 over-expression in 3T3-L1 adipocytes reduced insulin-stimulated glucose uptake. NYGGF4 over-expression impaired insulin-stimulated GLUT4 translocation without affecting the total protein content of GLUT4. The concentrations of TNF-α, IL-6, adiponectin and resistin in the culture medium of 3T3-L1 transfected with NYGGF4 were not significantly different from those in the control group. CONCLUSIONS: NYGGF4 over-expression impairs the insulin sensitivity of 3T3-L1 adipocytes through decreasing GLUT4 translocation and had no effects on the secretory function of adipocytes.［Chin J Contemp Pediatr, 2009, 11 (10):846-849］
ZHANG Chun-Mei,QIU Jie,CHEN Xiao-Hui et al. Effects of NYGGF4 gene over-expression on the insulin sensitivity and secretory function of adipocytes[J]. 中国当代儿科杂志, 2009, 11(10): 846-849.
ZHANG Chun-Mei,QIU Jie,CHEN Xiao-Hui et al. Effects of NYGGF4 gene over-expression on the insulin sensitivity and secretory function of adipocytes[J]. CJCP, 2009, 11(10): 846-849.
［1］Comuzzie AG, Allison DB. The search for human obesity genes［J］. Science, 1998, 280(5368):1374-1377.
［2］Rankinen T, Zuberi A, Chagnon YC, Weisnagel SJ, Argyropoulos G, Walts B, et al. The human obesity gene map:the 2005 update［J］. Obesity (Silver Spring), 2006, 14(4):529-644.
［3］Qiu J, Ni YH, Gong HX, Fei L, Pan XQ, Guo M, et al. Identification of differentially expressed genes in omental adipose tissues of obese patients by suppression subtractive hybridization［J］. Biochem Biophys Res Commun, 2007, 352(2):469-478.
［5］Chiba T, Yamaza H, Komatsu T, Nakayama M, Fujita S, Hayashi H, et al. Pituitary growth hormone suppression reduces resistin expression and enhances insulin effectiveness: relationship with caloric restriction［J］.Exp Gerontol, 2008, 43(6):595-600.
［6］Kaddai V, Jager J, Gonzalez T, Najem-Lendom R, Bonnafous S, Tran A, et al. Involvement of TNF-alpha in abnormal adipocyte and muscle sortilin expression in obese mice and humans［J］.Diabetologia, 2009, 52(5):932-940.
［7］Wang P, Mariman E, Renes J, Keijer J. The secretory function of adipocytes in the physiology of white adipose tissue［J］. J Cell Physiol, 2008, 216(1):3-13.
［8］Wang B, Zhang M, Ni YH, Liu F, Fan HQ, Fei L, et al. Identification and characterization of NYGGF4, a novel gene containing a phosphotyrosinebinding (PTB) domain that stimulates 3T3-L1 preadipocytes proliferation［J］. Gene, 2006, 379:132-140.
［9］Bergman RN, Kim SP, Catalano KJ, Hsu IR, Chiu JD, Kabir M, et al. Why visceral fat is bad: Mechanism of the metabolic syndrome ［J］. Obesity (Silver Spring), 2006, 14 (Supp1):S16-S19.
［10］Fan HQ, Gu N, Liu F, Fei L, Pan XQ, Guo M, et al. Prolonged exposure to resistin inhibits glucose uptake in rat skeletal muscles［J］. Acta Pharmacologica Sinica, 2007, 28(3)：410-416.
［11］Bryant NJ, Govers R, James DE. Regulated transport of the glucose transporter GLUT4［J］. Nat Rev Mol Cell Biol, 2002, 3(4):267-277.
［12］Kanzaki M. Insulin receptor signals regulating GLUT4 translocation and actin dynamics［J］. Endocr J, 2006, 53(3):267-293.
