www.thelancet.com/neurology Vol 16 October 2017 773 association between H pylori infection and insulin resistance or metabolic syndrome and associated comorbidities. These co-morbidities i n c l u d e a b d o m i n a l o b e s i t y, type 2 diabetes mellitus, dyslipidemia, hypertension (as mentioned by the authors), non-alcoholic fatty liver disease, and cardio-cerebrovascular disease, the endpoint of metabolic syndrome. An association between H pylori infection and metabolic syndrome is an appealing hypothesis, given that H pylori prevalence remains high in many regions, including south and east Europe, south America, and Asia; H pylori eradication might, therefore, have therapeutic beneficial effects on metabolic syndrome-related morbidities. Corroborating this association, the co-morbidities of metabolic syndrome related to H pylori infection appear to have crucial roles in the development of systemic diseases, including Alzheimer’s disease, Parkinson’s disease, glaucoma, other CNS and PNS neurodegenerative diseases, and some malignancies. H pylori infection and insulin resistance, the major underlying mechanism responsible for metabolic syndrome, appear to share common pathogenetic mediators in a milieu of chronic inflammatory and prothrombotic states, and oxidative stress; alterations to the concentrations of cytokines and adipokines involved in metabolic syndrome occur also in neurodegenerative disorders and many cancers. H pylori might contribute to neurodegeneration by promoting metabolic syndromerelated platelet–leucocyte aggregation. This aggregation might play a role in in the development of mild cognitive impairment and Alzheimer’s disease, for instance, by producing metabolic syndrome-associated reactive oxygen metabolites and circulating lipid peroxides associated with Alzheimer’s disease; by causing the development of cross-mimicry between endothelial and H pylori antigens; by increasing concentrations of metabolic syndrome-related homocysteine, a risk factor for brain pathologies that is implicated in endothelial damage and neurodegeneration via oxidative injury; or by affecting apoptosis. Moreover, we have shown that H pylori eradication can affect the clinical manifestations of Alzheimer’s disease and 5-year survival rates, which suggests that H pylori might be a causative factor in neurodegeneration. Further understanding of the mechanisms of H pylori-related metabolic syndrome in CNS and PNS injuries might have novel therapeutic implications and a marked effect on public health in the future.

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肥胖与神经系统：更多问题

www.thelancet.com/neurology Vol 16 October 2017 773 幽门螺杆菌感染与胰岛素抵抗或代谢综合征及相关合并症之间的关联。这些合并症包括腹部肥胖、2 型糖尿病、血脂异常、高血压（如作者所述）、非酒精性脂肪肝和心脑血管疾病（代谢综合征的终点）。鉴于幽门螺杆菌感染率在许多地区仍然很高，包括南欧和东欧、南美洲和亚洲，因此幽门螺杆菌感染与代谢综合征之间存在关联是一个有吸引力的假设。因此，根除幽门螺杆菌可能对代谢综合征相关的发病率产生有益的治疗效果。证实这个协会，与幽门螺杆菌感染相关的代谢综合征的共病似乎在全身性疾病的发展中起着至关重要的作用，包括阿尔茨海默病、帕金森病、青光眼、其他 CNS 和 PNS 神经退行性疾病以及一些恶性肿瘤。幽门螺杆菌感染和胰岛素抵抗是导致代谢综合征的主要潜在机制，在慢性炎症和血栓前状态以及氧化应激的环境中似乎具有共同的致病介质；参与代谢综合征的细胞因子和脂肪因子浓度的改变也发生在神经退行性疾病和许多癌症中。幽门螺杆菌可能通过促进代谢综合征相关的血小板 - 白细胞聚集而导致神经变性。这种聚集可能在轻度认知障碍和阿尔茨海默病的发展中发挥作用，例如，通过产生与代谢综合征相关的活性氧代谢物和与阿尔茨海默病相关的循环脂质过氧化物；通过引起内皮和幽门螺杆菌抗原之间交叉模拟的发展；通过增加与代谢综合征相关的同型半胱氨酸的浓度，这是一种脑病理的危险因素，与氧化损伤引起的内皮损伤和神经变性有关；或通过影响细胞凋亡。此外，我们已经表明，H pylori 根除可以影响阿尔茨海默病的临床表现和 5 年生存率，这表明 H pylori 可能是神经退行性疾病的致病因素。