Florkowski Melanie, Abiona Esther, Frank Karen M, Brichacek Allison L
Department of Laboratory Medicine, National Institutes of Health Clinical Center, Bethesda, MD, United States.
Front Nutr. 2024 Jun 24;11:1392666. doi: 10.3389/fnut.2024.1392666. eCollection 2024.
The prevalence of obesity has increased dramatically worldwide and has become a critical public health priority. Obesity is associated with many co-morbid conditions, including hypertension, diabetes, and cardiovascular disease. Although the physiology of obesity is complex, a healthy diet and sufficient exercise are two elements known to be critical to combating this condition. Years of research on the Mediterranean diet, which is high in fresh fruits and vegetables, nuts, fish, and olive oil, have demonstrated a reduction in numerous non-communicable chronic diseases associated with this diet. There is strong evidence to support an anti-inflammatory effect of the diet, and inflammation is a key driver of obesity. Changes in diet alter the gut microbiota which are intricately intertwined with human physiology, as gut microbiota-derived metabolites play a key role in biological pathways throughout the body. This review will summarize recent published studies that examine the potential role of gut metabolites, including short-chain fatty acids, bile acids, trimethylamine-N-oxide, and lipopolysaccharide, in modulating inflammation after consumption of a Mediterranean-like diet. These metabolites modulate pathways of inflammation through the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, toll-like receptor 4 signaling, and macrophage driven effects in adipocytes, among other mechanisms.
肥胖症在全球范围内的患病率急剧上升,已成为公共卫生的关键优先事项。肥胖与许多合并症有关,包括高血压、糖尿病和心血管疾病。尽管肥胖的生理机制很复杂,但健康饮食和充足运动是对抗这种情况的两个关键要素。对地中海饮食的多年研究表明,这种饮食富含新鲜水果、蔬菜、坚果、鱼类和橄榄油,与多种非传染性慢性病的减少有关。有强有力的证据支持这种饮食具有抗炎作用,而炎症是肥胖的关键驱动因素。饮食变化会改变肠道微生物群,而肠道微生物群与人体生理密切相关,因为肠道微生物群衍生的代谢产物在全身的生物途径中起着关键作用。本综述将总结最近发表的研究,这些研究探讨了肠道代谢产物,包括短链脂肪酸、胆汁酸、氧化三甲胺和脂多糖,在食用类似地中海饮食后调节炎症中的潜在作用。这些代谢产物通过含NOD样受体家族pyrin结构域3(NLRP3)炎性小体、Toll样受体4信号传导以及巨噬细胞对脂肪细胞的驱动作用等机制来调节炎症途径。