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http://dx.doi.org/10.7314/APJCP.2014.15.14.5895

Association of Polymorphisms in Stress-Related TNFα and NPY Genes with the Metabolic Syndrome in Han and Hui Ethnic Groups  

Bu, De-Yun (Public Health School, Ningxia Medical University)
Ji, Wen-Wu (Public Health School, Ningxia Medical University)
Bai, Dan (Public Health School, Ningxia Medical University)
Zhou, Jian (Public Health School, Ningxia Medical University)
Li, Hai-Xia (Public Health School, Ningxia Medical University)
Yang, Hui-Fang (Public Health School, Ningxia Medical University)
Publication Information
Asian Pacific Journal of Cancer Prevention / v.15, no.14, 2014 , pp. 5895-5900 More about this Journal
Abstract
Background: Metabolic syndrome (MS) is a cluster of complicated disorders caused by the interactive influencing factors of heredity and environment, which predisposes to many cnacers. Results from epidemic research indicate that stress is tightly related to the pathogenesis of MS and neoplasia. This paper aims to investigate the association between psychological stress and MS with respect to the tumor necrosis factor alpha (TNF${\alpha}$) and neuropeptide Y (NPY) genes in the Han and Hui ethnic groups. Methods: All subjects for this case-control study matched strict enrollment criteria (nationality, gender and age) and lived in the city of Wu Zhong of Ningxia Province in China. The enrolled group contained 102 matched pairs of Hui ethnic individuals and 98 matched pairs of Han ethnic individuals. Enrolled subjects completed the general Symptom Checklist-90 (SCL-90). The TNF${\alpha}$-308G/A variant and NPYrs16147 polymorphism were detected in case (81 males, 119 females) and control (81 males, 119 females) groups by polymerase chain reaction (PCR) amplification. Results: Nine factors of the SCL-90 were found to be statistically different (p<0.05) between case and control groups. The homozygous mutant genotype (AA) and the mutant allele (A) of the TNF${\alpha}$-308G/A gene were less frequently observed in the control population compared to the case group. The odds ratio (95% confidence interval) in "Allele" for MS was 2.28 (1.47-3.53), p=0.0001, while "OR" was 1.11 (0.83-1.47), p=0.15, for the NPYrs16147 gene polymorphism. Conclusions: Psychological stress has been positively associated with MS. A previous study from our group suggested there were differences in the level of psychological stress between Hui and Han ethnic groups. Furthermore, we found that the stress-related TNF${\alpha}$ gene was associated with MS for both Han and Hui ethnic groups. In contrast, NPY may be a possible contributor to MS and associated cancer for the Han ethnic group.
Keywords
Metabolic syndrome; psychological stress; TNF${\alpha}$-308G/A; NPYrs16147; SCL-90; Han and Hui ethnicity;
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1 Almadi T, Cathers I, Chow CM (2013). Associations among work-related stress, cortisol, inflammation and metabolic syndrome. Psychophysiology, 50, 821-30.   DOI
2 Black PH (2003). The inflammatory response is an integral part of the stress response: Implications for atherosclerosis, insulin resistance, type II diabetes and metabolic syndrome X. Brain Behav Immun, 17, 350-64.   DOI
3 Bose M, Olivan B, Laferrere B (2009). Stress and obesity: the role of the hypothalamic-pituitary-adrenal axis in metabolic disease. Curr Opin Endocrinol Diabetes Obes, 16, 340-6,   DOI
4 Curti ML, Pires MM, Barros CR, et al (2012). Associations of the TNF-alpha -308 G/A, IL6 -174 G/C and AdipoQ 45 T/G polymorphisms with inflammatory and metabolic responses to lifestyle intervention in Brazilians at high cardiometabolic risk. Diabetol Metab Syndr, 4, 49.   DOI
5 Dallman MF (2010). Stress-induced obesity and the emotional nervous system. Trends Endocrinol Metab, 21, 159-65.   DOI   ScienceOn
6 Dalziel B, Gosby AK, Richman RM, et al. (2002). Association of the TNF-alpha -308 G/A promoter polymorphism with insulin resistance in obesity. Obes Res, 10, 401-7.   DOI
7 Ferrannini E (2006). Is insulin resistance the cause of the metabolic syndrome? Ann Med, 38, 42-51, .   DOI
8 Fries E, Hesse J, Hellhammer J, et al (2005). A new view on hypocortisolism. Psychoneuroendocrinol, 30, 1010-6.   DOI   ScienceOn
9 Gallagher EJ, Leroith D, Karnieli E (2010). Insulin resistance in obesity as the underlying cause for the metabolic syndrome. Mt Sinai J Med, 77, 511-23.   DOI
10 Gehlert DR (1999). Role of hypothalamic neuropeptide Y in feeding and obesity. Neuropeptides, 33, 329-38.   DOI
11 Grundy SM, Brewer HJ, Cleeman JI, et al (2004). Definition of metabolic syndrome: Report of the National Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition. Circulation, 109, 433-8.   DOI   ScienceOn
12 Gulsun M, Tamam L, Ozcelik F (2012). Neuropeptide Y and Stress. Current Approaches Psychiatry, 4, 14-36.
13 Itokawa M, Arai M, Kato S, et al (2003). Association between a novel polymorphism in the promoter region of the neuropeptide Y gene and schizophrenia in humans. Neurosci Lett, 347, 202-4.   DOI
14 Gupta V, Gupta A, Jafar T, et al (2012). Association of TNFalpha promoter gene G-308A polymorphism with metabolic syndrome, insulin resistance, serum TNF-alpha and leptin levels in Indian adult women. Cytokine, 57, 32-6.   DOI
15 Haefliger JA, Waeber B, Grouzmann E, et al (1999). Cellular localization, expression and regulation of neuropeptide Y in kidneys of hypertensive rats. Regul Pept, 82, 35-43.   DOI
16 Heijboer AC, Voshol PJ, Donga E, et al (2005). High fat diet induced hepatic insulin resistance is not related to changes in hypothalamic mRNA expression of NPY, AgRP, POMC and CART in mice. Peptides, 26, 2554-8.   DOI
17 Jermendy G, Horvath T, Littvay L, et al (2011). Effect of genetic and environmental influences on cardiometabolic risk factors: a twin study. Cardiovasc Diabeto, 10, 96.   DOI
18 Kalra SP, Kalra PS (2004). NPY and cohorts in regulating appetite, obesity and metabolic syndrome: beneficial effects of gene therapy. Neuropeptides, 38, 201-11.   DOI
19 Kuo LE, Czarnecka M, Kitlinska JB, et al (2008). Chronic stress, combined with a high-fat/high-sugar diet, shifts sympathetic signaling toward neuropeptide Y and leads to obesity and the metabolic syndrome. Ann N Y Acad Sci, 1148, 232-7.   DOI   ScienceOn
20 Kuo LE, Kitlinska JB, Tilan JU, et al (2007). Neuropeptide Y acts directly in the periphery on fat tissue and mediates stress-induced obesity and metabolic syndrome. Nat Med, 13, 803-11.   DOI
21 Lo J, Bernstein LE, Canavan B, et al (2007). Effects of TNF-alpha neutralization on adipocytokines and skeletal muscle adiposity in the metabolic syndrome. Am J Physiol Endocrinol Metab, 293, 102-9.   DOI
22 Lee SC, Pu YB, Thomas GN, et al (2000). Tumor necrosis factor alpha gene G-308A polymorphism in the metabolic syndrome. Metabolism, 49, 1021-4.   DOI
23 Li L, Li X, Zhou W, et al (2013). Acute psychological stress results in the rapid development of insulin resistance. J Endocrinol, 217, 175-84.   DOI
24 Li YY (2012). Tumor necrosis factor-alpha g308alpha gene polymorphism and essential hypertension: a meta-analysis involving 2244 participants. PLoS One, 7, e35408.   DOI
25 McDermott BJ, Bell D (2007). NPY and cardiac diseases. Curr Top Med Chem, 7, 1692-03.   DOI
26 McEwen BS ( 1998). Protective and damaging effects of stress mediators. N Engl J Med, 338, 171-9.   DOI   ScienceOn
27 McGrowder D A, Jackson L A, Crawford T V, et al (2012). Prostate cancer and metabolic syndrome: is there a link. Asian Pac J Cancer Prev, 13, 1-13.   과학기술학회마을   DOI   ScienceOn
28 Meirhaeghe A, Cottel D, Amouyel P, et al (2005). Lack of association between certain candidate gene polymorphisms and the metabolic syndrome. Mol Genet Metab, 86, 293-9.   DOI
29 Moller DE. (2000). Potential role of TNF-alpha in the pathogenesis of insulin resistance and type 2 diabetes. Trends Endocrinol Metab, 11, 212-17.   DOI   ScienceOn
30 Morales-Medina JC, Dumont Y, Quirion R (2010). A possible role of neuropeptide Y in depression and stress. Brain Res, 1314, 194-05.   DOI
31 Rasmusson AM, Schnurr PP, Zukowska Z, et al (2010). Adaptation to extreme stress: post-traumatic stress disorder, neuropeptide Y and metabolic syndrome. Exp Biol Med (Maywood), 235, 1150-62.   DOI   ScienceOn
32 Nobili V, Bedogni G, Berni CR, et al (2012). The potential role of fatty liver in paediatric metabolic syndrome: a distinct phenotype with high metabolic risk? Pediatr Obes, 7, 75-80.   DOI
33 Olza J, Gil-Campos M, Leis R, et al (2013). Influence of variants in the NPY gene on obesity and metabolic syndrome features in Spanish children. Peptides, 45, 22-7.   DOI
34 Peltonen L (1999). Schizophrenia. All out for chromosome six. Nature, 378, 665-6.
35 Ronco AL1, De Stefani E, Deneo-Pellegrini H, et al (2012). Diabetes, overweight and risk of postmenopausal breast cancer: a case-control study in Uruguay. Asian Pac J Cancer Prev, 13, 139-46.   과학기술학회마을   DOI   ScienceOn
36 Ruohonen ST, Savontaus E, Rinne P, et al (2009). Stress-induced hypertension and increased sympathetic activity in mice overexpressing neuropeptide Y in noradrenergic neurons. Neuroendocrinology, 89, 351-60.   DOI
37 Saukkonen T, Jokelainen J, Timonen M, et al (2012). Prevalence of metabolic syndrome components among the elderly using three different definitions: a cohort study in Finland. Scand J Prim Health Care, 30, 29-34.   DOI
38 Song Y, Joung H (2012). A traditional Korean dietary pattern and metabolic syndrome abnormalities. Nutr Metab Cardiovasc Dis, 22, 456-62.   DOI   ScienceOn
39 Sookoian S, Garcia SI, Gianotti TF, et al (2005). The G-308A promoter variant of the tumor necrosis factor-alpha gene is associated with hypertension in adolescents harboring the metabolic syndrome. Am J Hypertens, 18, 1271-5.   DOI
40 Sookoian SC, Gonzalez C, Pirola CJ (2005). Meta-analysis on the G-308A tumor necrosis factor alpha gene variant and phenotypes associated with the metabolic syndrome. Obes Res, 13, 2122-31.   DOI
41 Teran-Garcia M, Bouchard C (2007). Genetics of the metabolic syndrome. Appl Physiol Nutr Metab, 32, 89-14.   DOI
42 Trayhurn P, Wood IS (2004). Adipokines: inflammation and the pleiotropic role of white adipose tissue. Br J Nutr, 92, 347-55.   DOI   ScienceOn
43 van Vliet M, von Rosenstiel IA, Schindhelm RK, et al (2009). Ethnic differences in cardiometabolic risk profile in an overweight/obese paediatric cohort in the Netherlands: a cross-sectional study. Cardiovasc Diabetol, 8, 2.   DOI
44 Vendrell J, Fernandez-Real JM, Gutierrez C, et al (2003). A polymorphism in the promoter of the tumor necrosis factoralpha gene (-308) is associated with coronary heart disease in type 2 diabetic patients. Atherosclerosis, 167, 257-64.   DOI
45 Maier, W, Schwab S, Rietschel M (2000). The genetics of schizophrenia. Curr Opin Psychiatry, 13, 3-9.   DOI
46 Zeggini E, Groves CJ, Parkinson JR, et al (2005). Large-scale studies of the association between variation at the TNF/LTA locus and susceptibility to type 2 diabetes. Diabetologia, 48, 2013-7.   DOI
47 Zhou Z, Zhu G, Hariri AR, et al (2008). Genetic variation in human NPY expression affects stress response and emotion. Nature, 452, 997-01.   DOI
48 Zukowska-Grojec Z. Neuropeptide Y (1995). A novel sympathetic stress hormone and more. Ann N Y Acad Sci, 771, 219-33.   DOI
49 Ozbek E, Otunctemur A, Dursun M, et al (2014). The metabolic syndrome is associated with more aggressive prostate cancer. Asian Pac J Cancer Prev, 15, 4029-32.   과학기술학회마을   DOI   ScienceOn