微生物组-肠道分离:肥胖起源的调查

IF 0.9 Q4 GASTROENTEROLOGY & HEPATOLOGY
David Smith, S. Jheeta
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引用次数: 5

摘要

减少超重仍然是一个重大的公共卫生挑战,目前控制仅限于减少卡路里的策略。目前,正在尝试重新审视基于Denis Burkitt的非洲研究的纤维假说,即现代饮食中缺乏膳食纤维是肥胖和他所说的“西方文明”的许多其他非传染性疾病发生的原因。然而,困境在于,伯基特本人强调,他那个时代的其他民族,如马赛人,在没有食用高纤维饮食的情况下仍然保持健康。同样,目前的肥胖流行病伴随着免疫系统失灵和心理健康不佳的疾病,而这些疾病似乎不能仅仅通过缺乏膳食纤维来充分解释。尽管在伯基特时代是未知的,但互惠肠道微生物组的日益退化将更符合观察到的流行病学,特别是如果微生物组在出生时不能有效地从母亲传给孩子的话。从更广泛的角度来看,在这篇文章中,我们认为微生物组是哺乳动物进化的辅助因子,其中母体微生物遗传补充了动物的母体遗传,两者都涉及表观遗传过程。由于这需要微生物组在动物发育成成虫时与动物完全融合,因此我们对微生物组-肠-脑轴具有重要的进化作用。由于未能正确建立微生物组-肠道界面,对母体微生物遗传的抑制为非传染性疾病的未来发展埋下了伏笔:一方面免疫系统功能受损,另一方面肠脑沟通失调。基本原理是,功能齐全、多样化的微生物组通过产生信使化学物质、信息化学物质来实现王国间的交流。可以设想,通过可摄入传感器原位检测这些尚未明确的化学实体将指示疾病的严重程度,并为其改善提供指导。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Microbiome–Gut Dissociation: Investigating the Origins of Obesity
The reduction of excessive weight remains a major public health challenge, with control currently limited to a calorie reduction strategy. Currently, attempts are being made at revisiting the fibre hypothesis based on the African studies of Denis Burkitt, that the lack of dietary fibre in the modern diet was responsible for the occurrence of obesity and many of the other non-communicable diseases of what he called “Western civilization”. However, the dilemma is that Burkitt himself stressed that other peoples of his day, such as the Maasai, remained healthy without consuming such high fibre diets. Equally, the present obesity epidemic is accompanied by diseases of a malfunctioning immune system and of poor mental health that do not seem to be adequately explained simply by a deficiency of dietary fibre. Though unknown in Burkitt’s day, an increasing degradation of a mutualistic intestinal microbiome would offer a better fit to the observed epidemiology, especially if the microbiome is not effectively passed on from mother to child at birth. Taking the broader view, in this article we posit a view of the microbiome as a cofactor of mammalian evolution, in which a maternal microbial inheritance complements the parental genetic inheritance of the animal, both engaging epigenetic processes. As this would require the microbiome to be fully integrated with the animal as it develops into an adult, so we have a meaningful evolutionary role for the microbiome–gut–brain axis. By a failure to correctly establish a microbiome–gut interface, the inhibition of maternal microbial inheritance sets the scene for the future development of non-communicable disease: compromised immune system function on the one hand and dysfunctional gut–brain communication on the other. The basic principle is that the fully functioning, diverse, microbiome achieves interkingdom communication by the generation of messenger chemicals, semiochemicals. It is envisaged that the in situ detection of these as yet ill-defined chemical entities by means of an ingestible sensor would indicate the severity of disease and provide a guide as to its amelioration.
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