• Expression of genes, which control glucose metabolism, in the blood of the obese boys with insulin resistance
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Expression of genes, which control glucose metabolism, in the blood of the obese boys with insulin resistance

SOVREMENNAYA PEDIATRIYA.2014.6(62):112-115;doi 10.15574/SP.2014.62.112

Expression of genes, which control glucose metabolism, in the blood of the obese boys with insulin resistance

Tiazhka O. V., Minchenko D. O., Davydov V. V., Moliavko O. S., Budreiko O. A., Kulieshova D. K., Minchenko O. H. 
National O.O. Bohomolets Medical University, Kyiv, Ukraine 
Palladin Institute of Biochemistry National Academy of Sciences of Ukraine, Kyiv, Ukraine 
SI «Institute of children and adolescent health care National Academy of Medical Science of Ukraine», Kharkiv, Ukraine

Objective: To study the expression of genes, which responsible for glycolytic glucose metabolism, in the blood of obese boys with and without of insulin resistance as well as in normal (control) individuals.

Materials and Methods. The 15 boys with mean age 14 years participate in this study. They were divided into three equal groups: normal individuals as control and patients with obesity and with or without insulin resistance. Glycolytic gene expressions were studied in blood cells using quantitative polymerase chain reaction.

Results. It was shown that the expression level of aldolase C (ALDOC) and (TIGAR) genes is increased, but ENO1 and ENO2 genes — significantly does not change in the blood cells of obese boys with normal insulin sensitivity as compared to control group. Insulin resistance in obese boys leads to down-regulation of ENO1 and ENO2 genes in the blood cells as compared to obese patients with normal insulin sensitivity.

Conclusions. Results of this study provide evidence that obesity affects the expression of the subset of glucose metabolism-related genes in the blood cells and that insulin resistance in obesity is associated with changes in the expression level of ENO1 and ENO2 genes, which contribute to the development of insulin resistance as well as glucose intolerance and may reflect the changes in fat tissue.

Key words: obesity, boys, insulin resistance, mRNA expression, ALDOC, TIGAR, ENO1, blood cells.

1. Song Y, Luo Q, Long H et al. 2014. Alpha-enolase as a potential cancer prognostic marker promotes cell growth, migration, and invasion in glioma. Mol Cancer. 13: 65.

2. Ruderman NB, Carling D, Prentki M, Cacicedo JM. 2013. AMPK, insulin resistance, and the metabolic syndrome. J Clin Invest. 123;7: 2764—2772.

3. Cheung EC, Ludwig RL, Vousden KH. 2012. Mitochondrial localization of TIGAR under hypoxia stimulates HK2 and lowers ROS and cell death. Proc Natl Acad Sci USA. 109;50: 20491—20496.

4. Huang W, Ramsey KM, Marcheva B, Bass J. 2011. Circadian rhythms, sleep, and metabolism. J Clin Invest. 121;6: 2133—2141.

5. Ozcan U, Cao Q, Yilmaz E, Lee AH et al. 2004. Endoplasmic reticulum stress links obesity, insulin action, and type 2 diabetes. Science. 306;5695: 457—461.

6. Bashta YM, Minchenko DO, Bova DO et al. 2014. Expression of protein phosphatase DUSP genes in subcutaneous adipose tissue of obese men with normal and impairment glucose tolerance. Biol Systems. 6;1: 3—9.

7. Gerin I, Noel G, Bolsee J, Haumont O et al. 2014. Identification of TP53-induced glycolysis and apoptosis regulator (TIGAR) as the phosphoglycolate-independent 2,3-bisphosphoglycerate phosphatase. Biochem J. 458;3: 439—448.

8. Ando H, Kumazaki M, Motosugi Y et al. 2011. Impairment of peripheral circadian clocks precedes metabolic abnormalities in ob/ob mice. Endocrinology. 152;4: 1347—1354.

9. Ye L, Zhao X, Lu J et al. 2013. Knockdown of TIGAR by RNA interference induces apoptosis and autophagy in HepG2 hepatocellular carcinoma cells. Biochem Biophys Res Commun. 437;2: 300—306.

10. Kovac J, Husse J, Oster H. 2009. A time to fast, a time to feast: the crosstalk between metabolism and the circadian clock. Mol Cells. 282: 75—80.

11. Lee J, Ozcan U. 2014. Unfolded Protein Response Signaling and Metabolic Diseases. J Biol Chem. 289;3: 1203—1211.

12. Minchenko OH, Kubaichuk KI, Minchenko DO et al. 2014. Molecular mechanisms of ERN1-mediated angiogenesis. Int J Physiol Pathophysiol. 5;1: 1-22.

13. Bochkov VN, Philippova M, Oskolkova O et al. 2006. Oxidized phospholipids stimulate angiogenesis via induction of VEGF, IL-8, COX-2 and ADAMTS-1 metalloprotease, implicating a novel role for lipid oxidation in progression and destabilization of atherosclerotic lesions. Circ Res. 99;8: 900—908.

14. Verhoef SP, Camps SG, Bouwman FG et al. 2013. Physiological response of adipocytes to weight loss and maintenance. PLoS One. 8;3: e58011.

15. Gao J, Zhao R, Xue Y et al. 2013. Role of enolase-1 in response to hypoxia in breast cancer: exploring the mechanisms of action. Oncol Rep. 29;4: 1322—1332.

16. Minchenko D, Ratushna O, Bashta Y et al. 2013. The expression of TIMP1, TIMP2, VCAN, SPARC, CLEC3B and E2F1 in subcutaneous adipose tissue of obese males and glucose intolerance. CellBio. 2;2: 25—33.