Arneth Borros
Institute of Laboratory Medicine and Pathobiochemistry, Molecular Diagnostics, Philipps University Marburg, Baldinger Str, Marburg, Germany.
Institute of Laboratory Medicine and Pathobiochemistry, Molecular Diagnostics, Justus Liebig University Giessen, Giessen, Germany.
Nutr Diabetes. 2025 Jun 10;15(1):26. doi: 10.1038/s41387-025-00383-w.
The endogenous intestinal microflora and environmental factors, such as diet, play central roles in immune homeostasis and reactivity. The microflora and diet both influence body weight and insulin resistance, notably through their effects on adipose cells. The aim of this study was to provide an update on how nutrient-derived factors (mostly focusing on fatty acids and glucose) impact the innate and acquired immune systems, including the immune system in the gut and its associated bacterial flora. The main source of fuel for energy-demanding immune cells is glucose. Insulin-responsive adipose tissue and Toll-like receptors (TLRs), which are part of the innate immune system and expressed in immune cells, intestinal cells, and adipocytes, are essential actors in the complex balance that ensures systemic immune and metabolic health. Leptin decreases during weight loss and increases brain activity in regions involved in the cognitive, emotional, and sensory control of food intake; restoring leptin levels maintains weight loss and reverses the alterations in brain activity. Obesity-triggering nutrients affect adipocytes, whereas proinflammatory leptin prompts the generation of cytokines and T cells. Collectively, data on nutrients demonstrate that starvation culminates in fat depletion, which then impacts the immune system. In people with obesity, inflammation originates largely from adipose tissue.
内源性肠道微生物群和环境因素，如饮食，在免疫稳态和反应性中起核心作用。微生物群和饮食都影响体重和胰岛素抵抗，特别是通过它们对脂肪细胞的作用。本研究的目的是提供关于营养衍生因子（主要关注脂肪酸和葡萄糖）如何影响先天性和获得性免疫系统的最新信息，包括肠道免疫系统及其相关细菌菌群。对能量需求较高的免疫细胞来说，葡萄糖是主要的能量来源。胰岛素反应性脂肪组织和Toll样受体（TLRs）是先天性免疫系统的一部分，在免疫细胞、肠道细胞和脂肪细胞中表达，它们是确保全身免疫和代谢健康的复杂平衡中的关键因素。减肥期间瘦素水平下降，而参与食物摄入认知、情绪和感觉控制的脑区活动增加；恢复瘦素水平可维持体重减轻并逆转脑活动的改变。引发肥胖的营养物质会影响脂肪细胞，而促炎瘦素会促使细胞因子和T细胞的产生。总体而言，关于营养物质的数据表明，饥饿最终导致脂肪消耗，进而影响免疫系统。在肥胖人群中，炎症主要源于脂肪组织。
