Fernández-Real José-Manuel, López-Bermejo Abel, Vendrell Joan, Ferri Maria-José, Recasens Mónica, Ricart Wifredo
Section of Diabetes, Endocrinology and Nutrition, Institut d'Investigació Biomédica de Girona, Avinguda de França s/n, 17007 Girona, Spain.
Diabetes Care. 2006 May;29(5):1058-64. doi: 10.2337/diacare.2951058.
We hypothesized that burden of infection could be associated with chronic low-grade inflammation, resulting in insulin resistance. We aimed to study the effect of exposure to four infections on insulin sensitivity in apparently healthy middle-aged men (n = 124).
By inclusion criteria, all subjects were hepatitis C virus antibody seronegative. Each study subject's serum was tested for specific IgG class antibodies against herpes simplex virus (HSV)-1, HSV-2, enteroviruses, and Chlamydia pneumoniae through the use of quantitative in vitro enzyme-linked immunosorbent assays. Insulin sensitivity was evaluated using minimal model analysis.
The HSV-2 titer was negatively associated with insulin sensitivity even after controlling for BMI, age, and C-reactive protein (CRP). The associations were stronger when considering the infection burden. In particular, in those subjects who were seropositive for C. pneumoniae, the relationship between the quantitative seropositivity index (a measure of the exposure to various pathogens) and insulin sensitivity was strengthened (r = -0.50, P < 0.0001). We also observed decreasing mean insulin sensitivity index with increasing seropositivity score in subjects positive for enteroviruses. In the latter, the relationship between insulin sensitivity and seropositivity was especially significant (r = -0.71, P < 0.0001). In a multivariate regression analysis, both BMI and quantitative seropositivity index (7%) independently predicted insulin sensitivity variance in subjects with C. pneumoniae seropositivity. When controlling for CRP, this association was no longer significant.
Pathogen burden showed the strongest association with insulin resistance, especially with enteroviruses and C. pneumoniae seropositivity. We hypothesize that exposure to multiple pathogens could cause a chronic low-grade inflammation, resulting in insulin resistance.
我们推测感染负担可能与慢性低度炎症相关，进而导致胰岛素抵抗。我们旨在研究暴露于四种感染对明显健康的中年男性（n = 124）胰岛素敏感性的影响。
根据纳入标准，所有受试者丙型肝炎病毒抗体血清学检测均为阴性。通过定量体外酶联免疫吸附试验检测每位研究对象血清中针对单纯疱疹病毒（HSV）-1、HSV-2、肠道病毒和肺炎衣原体的特异性IgG类抗体。使用最小模型分析评估胰岛素敏感性。
即使在控制了体重指数（BMI）、年龄和C反应蛋白（CRP）之后，HSV-2滴度仍与胰岛素敏感性呈负相关。考虑感染负担时，这种相关性更强。特别是，在肺炎衣原体血清学阳性的受试者中，定量血清学阳性指数（一种衡量接触各种病原体的指标）与胰岛素敏感性之间的关系得到加强（r = -0.50，P < 0.0001）。我们还观察到肠道病毒阳性受试者的平均胰岛素敏感性指数随血清学阳性评分增加而降低。在后者中，胰岛素敏感性与血清学阳性之间的关系尤为显著（r = -0.71，P < 0.0001）。在多变量回归分析中，BMI和定量血清学阳性指数（7%）独立预测肺炎衣原体血清学阳性受试者的胰岛素敏感性差异。在控制CRP后，这种关联不再显著。
病原体负担与胰岛素抵抗的关联最为强烈，尤其是与肠道病毒和肺炎衣原体血清学阳性相关。我们推测暴露于多种病原体会导致慢性低度炎症，进而导致胰岛素抵抗。
