Investigation of the Relationship Between Chronic Stress and Insulin Resistance in a Chinese Population

Overview

Journal J Epidemiol

Specialty Public Health

Date 2016 Feb 3

PMID 26830350

Citations 25

Authors

Yu-Xiang Yan

Huan-Bo Xiao

Si-Si Wang

Jing Zhao

Yan He

Wei Wang

Jing Dong

Affiliations

Soon will be listed here.

Abstract

Background: Chronic stress may facilitate the development of metabolic diseases. Insulin resistance is present long before the clinical manifestations of individual metabolic abnormalities. To explore whether chronic stress is an independent risk factor of insulin resistance, we investigated the relationship between the stress system, selected parameters of energy homeostasis, and insulin resistance in a Chinese population.

Methods: We recruited 766 workers employed at four companies in Beijing. The degree of insulin resistance was determined using the homeostasis model assessment of insulin resistance (HOMA-IR). The highest quartile of HOMA-IR among all study subjects was further defined as insulin resistance in our study. The short standard version of the Copenhagen Psychosocial Questionnaire (COPSOQ) was used to assess job-related psychosocial stress. Pearson's correlation coefficients were calculated between cortisol level and HOMA-IR and components of metabolic syndrome, with stratification by gender. The relationship between cortisol and HOMA-IR independent of obesity was analyzed using a linear mixed model with company as a cluster unit.

Results: The values of the two scales of COPSOQ, including "demands at work" and "insecurity at work", were significantly associated with insulin resistance and cortisol concentration (P < 0.05). Cortisol was significantly positively correlated with glucose, HOMA-IR, and waist circumference in males and females (P < 0.05). After adjusting for potential confounders, cortisol was an independent positive predictor for HOMA-IR (P < 0.05).

Conclusions: These findings showed that chronic stress was associated with insulin resistance and may contribute to the development of insulin resistance.

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References

Yan Y, Dong J, Zhang J, Liu F, Wang W, Zhang L . Polymorphisms in NR3C1 gene associated with risk of metabolic syndrome in a Chinese population. Endocrine. 2014; 47(3):740-8. DOI: 10.1007/s12020-014-0324-9. View

Kristensen T, Hannerz H, Hogh A, Borg V . The Copenhagen Psychosocial Questionnaire--a tool for the assessment and improvement of the psychosocial work environment. Scand J Work Environ Health. 2006; 31(6):438-49. DOI: 10.5271/sjweh.948. View

Bjorntorp P . Do stress reactions cause abdominal obesity and comorbidities?. Obes Rev. 2002; 2(2):73-86. DOI: 10.1046/j.1467-789x.2001.00027.x. View

Nicod N, Giusti V, Besse C, Tappy L . Metabolic adaptations to dexamethasone-induced insulin resistance in healthy volunteers. Obes Res. 2003; 11(5):625-31. DOI: 10.1038/oby.2003.90. View

Tamashiro K, Sakai R, Shively C, Karatsoreos I, Reagan L . Chronic stress, metabolism, and metabolic syndrome. Stress. 2011; 14(5):468-74. DOI: 10.3109/10253890.2011.606341. View

Li L, Guo Y, Chen Z, Chen J, Peto R . Epidemiology and the control of disease in China, with emphasis on the Chinese Biobank Study. Public Health. 2012; 126(3):210-213. PMC: 4340568. DOI: 10.1016/j.puhe.2011.11.012. View

Barthel A, Scherbaum W, Bornstein S . [Novel aspects in the mechanisms of steroid diabetes and the regulation of hepatic glucose production by insulin and steroids]. Med Klin (Munich). 2003; 98(5):283-6. DOI: 10.1007/s00063-003-1258-9. View

Monzillo L, Hamdy O . Evaluation of insulin sensitivity in clinical practice and in research settings. Nutr Rev. 2004; 61(12):397-412. DOI: 10.1301/nr.2003.dec.397-412. View

Caro J . Clinical review 26: Insulin resistance in obese and nonobese man. J Clin Endocrinol Metab. 1991; 73(4):691-5. DOI: 10.1210/jcem-73-4-691. View

10.

Ware W . Psychological stress, insulin resistance, inflammation and the assessment of heart disease risk. Time for a paradigm shift?. Med Hypotheses. 2008; 71(1):45-52. DOI: 10.1016/j.mehy.2008.02.008. View

11.

Buren J, Eriksson J . Is insulin resistance caused by defects in insulin's target cells or by a stressed mind?. Diabetes Metab Res Rev. 2005; 21(6):487-94. DOI: 10.1002/dmrr.567. View

12.

Lundgren M, Buren J, Ruge T, Myrnas T, Eriksson J . Glucocorticoids down-regulate glucose uptake capacity and insulin-signaling proteins in omental but not subcutaneous human adipocytes. J Clin Endocrinol Metab. 2004; 89(6):2989-97. DOI: 10.1210/jc.2003-031157. View

13.

Binnert C, Ruchat S, Nicod N, Tappy L . Dexamethasone-induced insulin resistance shows no gender difference in healthy humans. Diabetes Metab. 2004; 30(4):321-6. DOI: 10.1016/s1262-3636(07)70123-4. View

14.

Sjostrand M, Eriksson J . Neuroendocrine mechanisms in insulin resistance. Mol Cell Endocrinol. 2008; 297(1-2):104-11. DOI: 10.1016/j.mce.2008.05.010. View

15.

Novelli M, Pocai A, Chiellini C, Maffei M, Masiello P . Free fatty acids as mediators of adaptive compensatory responses to insulin resistance in dexamethasone-treated rats. Diabetes Metab Res Rev. 2007; 24(2):155-64. DOI: 10.1002/dmrr.785. View

16.

Yan Y, Dong J, Liu Y, Yang X, Li M, Shia G . Association of suboptimal health status and cardiovascular risk factors in urban Chinese workers. J Urban Health. 2011; 89(2):329-38. PMC: 3324604. DOI: 10.1007/s11524-011-9636-8. View

17.

McEwen B . Central effects of stress hormones in health and disease: Understanding the protective and damaging effects of stress and stress mediators. Eur J Pharmacol. 2008; 583(2-3):174-85. PMC: 2474765. DOI: 10.1016/j.ejphar.2007.11.071. View

18.

Eller N, Netterstrom B, Hansen A . Psychosocial factors at home and at work and levels of salivary cortisol. Biol Psychol. 2006; 73(3):280-7. DOI: 10.1016/j.biopsycho.2006.05.003. View

19.

Yan Y, Dong J, Liu Y, Zhang J, Song M, He Y . Association of suboptimal health status with psychosocial stress, plasma cortisol and mRNA expression of glucocorticoid receptor α/β in lymphocyte. Stress. 2014; 18(1):29-34. DOI: 10.3109/10253890.2014.999233. View

20.

Matthews D, Hosker J, Rudenski A, Naylor B, Treacher D, Turner R . Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985; 28(7):412-9. DOI: 10.1007/BF00280883. View