Progress in researches on mechanism of comorbidity of metabolic syndrome and depression
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摘要: 近年来随着代谢综合征发病率的升高,其并发抑郁症的人数也相应增加。代谢综合征中的胰岛素抵抗、皮质醇增多、免疫炎症活化、氧化应激和自主神经调节紊乱与抑郁症的发生有关,而抑郁症患者的不健康生活习惯又是发生代谢综合征的原因。探索二者之间的关系,有助于进一步研究其发病机制,预防和治疗代谢综合征相关性抑郁症。本文主要从流行病学、临床医学角度探讨代谢综合征和抑郁症的关系及两病共病的可能病理生理机制。现有研究提示,多种遗传和环境因素及其相互作用与其发病相关,但确切发病机制尚不清楚。Abstract: In recent years, with the increased incidence of metabolic syndrome (MS), the number of MS patients with depression has increased accordingly. Insulin resistance, cortisol increase, immune inflammation activation, oxidative stress and autonomic nervous regulation disorder in MS are related to the occurrence of depression, and unhealthy living habits of depressive patients are the causes of MS. Exploring the relationship between the two diseases is helpful to study the pathogenesis of the diseases for the prevention and treatment of MS-related depression. The study mainly discusses the relationship between MS and depression based on epidemiological and clinical studies, and then summarizes the possible pathophysiological mechanism of comorbidity of MS and depression. Published studies suggest that the co-pathogenesis of MS and depression is caused by the interaction of multiple genetic and environmental factors but specific pathogenesis is still unclear and needs further study.
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Key words:
- metabolic syndrome /
- depression /
- comorbidity mechanism
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[1] Räikkönen K, Matthews KA, Kuller LH. Depressive symptoms and stressful life events predict metabolic syndrome among middle-aged women: a comparison of World Health Organization, Adult Treatment Panel III, and International Diabetes Foundation definitions[J]. Diabetes Care, 2017, 30(11): 872 – 877. [2] Koponen H, Jokelainen J, Keinänen-Kiukaanniemi S, et al. Metabolic syndrome predisposes to depressive symptoms: a population-based 7-year follow-up study[J]. Clin Psychiatry, 2018, 23(8): e1 – e5. [3] Räikkönen K, Matthews KA, Kuller LH. The relationship between psychological risk attributes and the metabolic syndrome in healthy women: antecedent or consequence?[J]. Metabolism, 2012, 51(9): 1573 – 1577. [4] McCaffery JM, Niaura R, Todaro JF, et al. Depressive symptoms and metabolic risk in adult male twins enrolled in the National Heart, Lung, and Blood Institute twin study[J]. Psychosom Med, 2013, 65(6): 490 – 497. [5] Skilton MR, Moulin P, Terra JL, et al. Associations between anxiety, depression, and the metabolic syndrome[J]. Biol Psychiatry, 2019, 62(7): 1251 – 1257. [6] Frasure-Smith N, Lesperance F, Talajic M. Depression following myocardial infarction. Impact on 6-month survival[J]. JAMA, 2017, 270(3): 1819 – 1825. [7] Osby U, Brandt L, Correia N, et al. Excess mortality in bipolar and unipolar disorder in Sweden[J]. Arch Gen Psychiatry, 2018, 582(8): 844 – 850. [8] Kashyap S, Belfort R, Gastaldelli A, et al. A sustained increase in plasma free fatty acids impairs insulin secretion in nondiabetic subjects genetically predisposed to develop type 2 diabetes[J]. Diabetes, 2013, 52(2): 2461 – 2474. [9] Reaven GM. Banting lecture 1988: role of insulin resistance in human disease[J]. Diabetes, 2018, 37(9): 1595 – 1607. [10] Sarafi dis PA, Bakris GL. Non-esterified fatty acids and blood pressure elevation: a mechanism for hypertension in subjects with obesity/insulin resistance?[J]. Hum Hypertens, 2017, 21(5): 12 – 19. [11] McIntyre RS, Konarski JZ, Wilkins K, et al. Obesity in bipolar disorder and major depressive disorder: results from a national community health survey on mental health and well-being[J]. Can J Psychiatry, 2016, 51(12): 274 – 280. [12] Lapidus L, Bengtsson C, Larsson B, et al. Distribution of adipose tissue and risk of cardiovascular disease and death: a 12 year follow up of participants in the population study of women in Gothenburg, Sweden[J]. Br Med J (Clin Res Ed), 2018, 289(4): 1257 – 1261. [13] Kalkhoff RK, Hartz AH, Rupley D, et al. Relationship of body fat distribution to blood pressure, carbohydrate tolerance, and plasma lipids in healthy obese women[J]. J Lab ClinMed, 2018, 102(2): 621 – 627. [14] Moreira RO, Marca KF, Appolinario JC, et al. Increased waist circumference is associated with an increased prevalence of mood disorders and depressive symptoms in obese women[J]. Eat Weight Disord, 2017, 12(9): 35 – 40. [15] Southwick SM, Vythilingam M, Charney DS. The psychobiology of depression and resilience to stress: implications for prevention and treatment[J]. Annu Rev ClinPsychol, 2015, 1(12): 255 – 291. [16] Banki CM, Karmacsi L, Bissette G, et al. CSF corticotropin-releasing hormone and somatostatin in major depression: response to antidepressant treatment and relapse[J]. Eur Neuropsychopharmacol, 2018, 2(11): 107 – 113. [17] Kapczinski F, Vieta E, Andreazza AC, et al. Allostatic load in bipolar disorder: implications for pathophysiology and treatment[J]. Neurosci Biobehav Rev, 2018, 32(20): 675 – 692. [18] McIntyre RS, Soczynska JK, Konarski JZ, et al. Should depressive syndromes be reclassified as “metabolic syndrome type II”?[J]. Ann Clin Psychiatry, 2017, 19(8): 257 – 264. [19] Craft S, Watson GS. Insulin and neurodegenerative disease: shared and specifi c mechanisms[J]. Lancet Neurol, 2014, 3(10): 169 – 178. [20] Girgis RR, Javitch JA, Lieberman JA. Antipsychotic drug mechanisms: links between therapeutic effects, metabolic side effects and the insulin signaling pathway[J]. Mol Psychiatry, 2018, 13(20): 918 – 929. [21] Gould TD, Manji HK. Glycogen synthase kinase-3: a putative molecular target for lithium mimetic drugs[J]. Neuropsychopharmacology, 2018, 30(8): 1223 – 1237. [22] Raison CL, Capuron L, Miller AH. Cytokines sing the blues: inflammation and the pathogenesis of depression[J]. Trends Immunol, 2016, 27(4): 24 – 31. [23] Kiecolt-Glaser JK, Glaser R. Depression and immune function: central pathways to morbidity and mortality[J]. Psychosom Res, 2012, 53(1): 873 – 876. [24] Selley ML. Increased (E)-4-hydroxy-2-nonenal and asymmetric dimethylarginine concentrations and decreased nitric oxide concentrations in the plasma of patients with major depression[J]. Affect Disord, 2014, 80(20): 249 – 256. [25] Sarandol A, Sarandol E, Eker SS, et al. Major depressive disorder is accompanied with oxidative stress: short-term antidepressant treatment does not alter oxidative-antioxidative systems[J]. Hum Psychopharmacol, 2017, 22(30): 67 – 73. [26] Sarandol A, Sarandol E, Eker SS, et al. Oxidation of apolipoprotein B-containing lipoproteins and serum paraoxonase/arylesterase activities in major depressive disorder[J]. Prog Neuropsychopharmacol Biol Psychiatry, 2016, 30(9): 1113 – 1118. [27] Maiese K, Morhan SD, Chong ZZ. Oxidative stress biology and cell injury during type 1 and type 2 diabetes mellitus[J]. Curr Neurovasc Res, 2017, 4(30): 63 – 71. [28] Forlenza MJ, Miller GE. Increased serum levels of 8-hydroxy-2’ -deoxyguanosine in clinical depression[J]. Psychosom Med, 2016, 68(21): 1 – 7. [29] Carney RM, Freedland KE, Veith RC. Depression, the autonomic nervous system, and coronary heart disease[J]. Psychosom Med, 2018, 67(Suppl 1): S29 – S33. [30] Carnethon MR, Golden SH, Folsom AR, et al. Prospective investigation of autonomic nervous system function and the development of type 2 diabetes: the Atherosclerosis Risk In Communities study, 1987-1998[J]. Circulation Med, 2013, 107(8): 2190 – 2195. [31] Golden RN, Markey SP, Risby ED, et al. Antidepressants reduce whole-body norepinephrine turnover while enhancing 6-hydroxymelatonin output[J]. Arch Gen Psychiatry, 2018, 45(18): 150 – 154. [32] Benthem L, Keizer K, Wiegman CH, et al. Excess portal venous long-chain fatty acids induce syndrome X via HPA axis and sympathetic activation[J]. Am J Physiol Endocrinol Metab, 2016, 279(2): E1286 – E1293.
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