有一些研究职员将肠道菌群描述为：与宿主代谢密切干系的附加环境特色143。只管有了这些证据，但肠道菌群在肥胖中的浸染仍旧是一个相称新颖的观点，须要进一步的研究来确定肠道菌群在肥胖发展和治疗策略中的浸染。
肠道菌群彷佛反响了一个人的生活办法；然而，肠道菌群的变革究竟是肥胖的缘故原由还是结果，还须要更深入的研究。
有趣的是，碳水化合物（即纤维）、蛋白质和脂肪的摄入会影响粪便微生物，这一征象解释宏量营养素与微生物之间存在互作144。只管有了这些数据，但是每个个体的微生物组组成都是独特的，是个体代谢和体重状态的代表性特色144,145。
首创性的研究已经描述了微生物组与肥胖之间的关系。详细地说，数据显示肥胖小鼠的厚壁菌（Firmicutes）增多，拟杆菌（Bacteroidetes）减少，这表明这些微生物对宿主代谢可能有影响146。另一项人类研究的研究职员比较了来自体型纤瘦者和肥胖者的微生物样本，证明了上述结果145。
一些研究职员创造，肥胖者从食品中得到的能量增加，并且这些人的粪便样本中普氏菌（Prevotellaceae）和古细菌（Archaea）增多147。此外，细菌丰度和多样性与肥胖呈负干系，即细菌丰度低的个体会涌现更严重的肥胖、胰岛素抵抗和血脂非常，以及轻度的全身炎症144。其他的研究也揭示了肠道细菌，如 Akkermansia muciniphila，对内源性大麻素系统以及体重、食品摄入的调节148。
然而，肥胖者的肠道微生物群特色显示出广泛的差异性，这是由多个成分调节的，包括宏量营养素的摄入。例如，一项人类研究报告了与肥胖干系的肠道菌群存在性别差异149。此外，其他研究职员也提出，肠道菌群的差异取决于遗传差异150。然而，肠道菌群的组成已被证明紧张受饮食中营养身分（表 2）的调节151。
考虑到这一点，独特微生物群落（被称为“肠型”）的鉴定及其与康健和疾病的关系表明，肠道菌群在临床常规考验中的运器具有主要浸染。通过研究这些特性，研究职员可以更好地理解糖和纤维在肠道微生态平衡和失落调中的不同浸染，以及这些浸染如何影响患者预后和微生物组的功能152。
能量回收的差异彷佛是由细菌产生的短链脂肪酸引起的，它提高了消化废物（习气性消化的残余物）的能量利用率153。同样，短链脂肪酸对宿主的影响也与能量花费有关，它可以调节产热干系基因（如 PPARG 或 UCP2）的表达和增强脂质氧化154。
此外，短链脂肪酸也会影响超重人群的食欲，调控食品摄入干系的短期通路；给结肠输注短链脂肪酸稠浊物，会增加血浆 PYY 水平，这是由上皮 G 蛋白偶联受体（GPR41 和 GPR43）激活所触发的155。然而，短链脂肪酸含量与粪便中细菌丰度之间的关系仍不清楚。未来的人类干预研究将有助于确定：微生物的发酵和能源利用对掌握体重和肥胖症的长期效益。
饮食中宏量营养素发酵产生的代谢产物对肥胖及并发症的影响已被广泛研究158。碳水化合物的摄入被描述为调节肠道菌群的紧张成分159,160。纤维通过调节食品在胃肠道中的转运、葡萄糖接管和粪便膨胀发挥浸染，从而影响血糖反应和饱腹感旗子暗记161,162。
此外，可发酵伙食纤维在调节肠道菌群中具有关键浸染158。益生元，如低聚果糖，对肠道菌群的影响已经被一些研究证明，低聚果糖可以调节 Faecali bacteriumprausnitzii和其他细菌的丰度，并与丁酸的产生干系，丁酸可以通过降落下丘脑神经肽Y的表达而减少食品的摄入163。
还有研究调查了富含糖和人工甜味剂的“西方”饮食对肠道菌群组成的影响7。不幸的是，甜味剂和肥胖者肠道菌群之间的联系仍旧不清楚。个中一项小鼠研究表明，西方饮食模式更受厚壁菌（Firmicutes）的青睐，并且在小鼠体内，与果糖和甘露糖代谢、糖酵解和糖异生干系的基因表达增加164。
一项对人类的不雅观察研究表明，肥胖人群中也存在小肠细菌的增长的征象，这些肥胖人群的饮食中富含碳水化合物和精制糖，但缺少纤维165。
伙食蛋白质和碳水化合物对肠道菌群的调节浸染改变了蛋白质消化的衍生物166。这些衍生物通过改变芳香族和支链氨基酸的发酵，以及作为短链脂肪酸的前体，影响能量代谢167。
例如，当肠道中的碳水化合物水平较低时，肠道细菌可以改变发酵的底物168。这种情形促进了蛋白质的发酵和分解代谢，从而改变肠道 pH 值、转运韶光（大量食品从进入肠道到渗出的韶光）和微生物组168。
在这方面，一项包括肥胖者的试验表明，在高蛋白饮食后，肠道中短链脂肪酸的浓度降落，Roseburia 和 Eubacteriumrectale 的丰度减少，支链氨基酸、苯乙酸和 N-亚硝基化合物的增加，从而可能会对宿主康健产生有害影响169。
而另一篇综述强调了特定氨基酸的抗炎浸染，它们通过肠道菌群产生的色氨酸衍生物来增强肠道的樊篱功能170。此外，该综述的作者还宣布了 GLP1 对宿主代谢的调节浸染，以及由色氨酸的肠道菌群代谢产物吲哚引起的饱足感170。
此外，其他研究职员认为，除了能量平衡外，其他成分也会改变伙食脂肪摄入对体重增加的影响171。高脂饮食可以通过抗菌浸染影响肠道菌群，匆匆使微生物组失落调，这种失落调与肥胖导致的全身匆匆炎症状态干系171。
对康健人进行的横断面研究创造，拟杆菌（Bacteroidetes）和放线菌（Actinobacteria）与习气性饮食中的脂肪摄入呈正干系172。此外，该研究还揭示了，与体重指数（BMI）干系的微生物也与饱和脂肪酸的热量摄入干系172。
另一项调查同卵双胞胎脂肪摄入质量的研究创造，单不饱和脂肪酸与双歧杆菌（Bifidobacterium）和拟杆菌（Bacteroidetes）的丰度正干系；n-3 多不饱和脂肪酸与乳酸杆菌（Lactobacillus）之间存在正干系关系；而 n-6 多不饱和脂肪酸与双歧杆菌（Bifidobacterium）之间则负干系173。
然而，一些研究职员认为，在饮食中添加益生菌可以减轻伙食脂肪对体重坚持和脂肪积累的不利影响174,175。
肥胖的综合研究
精准营养与精准医学已成为体重坚持与肥胖管理的主要课题。在精准营养与精准医学中，个性化不仅包括代谢表型、食品偏好、临床病史或生活办法，还包括新兴的个性化标准，个中基因型和肠道菌群的组成是定制疾病治疗方案的根本，特殊是代谢紊乱。
因此，越来越多的研究职员开始对饮食模式感兴趣，开始研究食品营养素、肠道菌群的组成和遗传背景之间繁芜的相互浸染对肥胖的影响176。
一项对照饮食试验将康健人分为两组，一组食用高脂肪低纤维饮食，另一组食用低脂肪高纤维饮食，在饮食干预 24 小时后，研究职员创造参与者的肠道菌群组成发生了变革，这些变革在研究的 10 天内保持稳定172。
研究职员还报告了长期饮食模式和菌群之间的关系。详细地，他们宣布了蛋白质、动物脂肪与拟杆菌（Bacteroidetes），碳水化合物与普氏菌（Prevotella）之间的关系172。
同样，其他营养干预研究也创造，大鼠高脂高糖或低脂高糖饮食后，细菌的多样性低落。这些饮食与肠道炎症的增加、迷走神经的肠-脑联系改变有关，从而使得身体脂肪沉积增加177。
一些研究职员强调了肠道微生物种群综合剖析和代谢组学剖析的运用前景，这些剖析可以客不雅观评估康健饮食模式的可循性，并帮助阐明这些模式（如地中海饮食模式）中的明确饮食身分，以及它们在心脏代谢紊乱发展的繁芜相互浸染中可能的影响178。
例如，一项试验报告了肥胖者肠道菌群组成与康健饮食状况干系的差异179。更详细地说，那些饮食摄入更康健的人，肠道微生物的丰度更高，炎症标志物的浓度更低179。同样，一些研究职员强调须要进一步调查，以确定细菌对特定饮食干预的反应，以及对宿主代谢的有益影响180,181。
然而，这须要新的代谢标志物或新技能，来帮助阐明特定饮食的营养摄入，以制订更详细的营养评估，并确定它们如何影响肠道菌群和遗传之间的互作。这样的技能将使我们能够更准确地确定：宏量营养素对与肥胖发展有关的代谢通路和内分泌旗子暗记的特定影响。
事实上，一些研究已经证明了，宿主基因型和肠道菌群与内脏脂肪的关系39,182。一个研究团队创造低热量高蛋白饮食对 BMI 超重组中有双歧杆菌干系 LCT 基因型变异（LCT 编码乳糖酶）的个体有益150。
在这些研究的根本上，数据表明饮食成分之间的相互浸染与肥胖中创造的代谢损伤有关，如宏量营养素分布、肠道菌群组成和遗传背景25。对个体特色和肠道菌群代谢物干系敏感性的整体研究有助于制订新的营养评估策略，以提高肥胖的预防和治疗效果183。
对这一课题的进一步研究应旨在确定：依赖于特定肠型、人体康健代谢产物、能量平衡和体重掌握158的筛选和检测工具，以增强预防和治疗肥胖的临床实践的个性化184。由于研究的终极目的是发展完善的精准营养咨询，以是须要开展进一步的研究，以更好地理解肥胖发展过程中所涉及的繁芜相互浸染。
这项研究在进行之前须要在整合所有的个体信息以及生物学数据，这些个体信息包括：生活办法及环境、文化、临床病史（包括药物、过敏和不耐受的不良影响）、体力活动水平、就寝及饮食模式、食品偏好和行为成分（即暴露组）；这些生物学数据包括：昼夜节律、遗传学、表不雅观遗传学、亚基因组学和代谢组学。
结论在理解体脂沉积和体重稳定性方面，宏量营养素摄入分布和伙食组成正成为主要的研究领域。科学进展表明，为了对抗肥胖症盛行，科学家不仅须要考虑碳水化合物、蛋白质和脂质的分外贡献，还须要考虑单一氨基酸、脂肪酸和各种碳水化合物衍生的分子，以及它们与遗传背景和肠道菌群的相互浸染——这是精准营养和医学的根本。
脂肪和糖，作为紧张的产能营养素，它们的摄入被认为是肥胖症盛行的紧张驱出发分，由于两者都有助于能量的供应。然而，由于它们参与到共同的、与能量稳态干系的代谢通路51，想要从现有证据中阐明每种宏量营养素对肥胖的单独贡献是一项寻衅。
这一问题乃至比想得更加繁芜，由于能量代谢方面的繁芜相互浸染，以及每个个体综合代谢的灵巧性，使得人类能够根据自身对营养素的可用性和须要，合理利用不同来源的能量62。换言之，很难说脂肪比糖更有害，由于整体的能量摄入与花费，可能比使体重增加的特定能量来源更主要。
然而，特定脂肪酸和糖的浸染可能阐明了能量效率的一些差异，而蛋白质彷佛可以减少食欲和促进产热，对体重坚持有积极浸染56。
过度的体重和脂肪组织的积累依赖于能量平衡，摄入的宏量营养素产能长期高于能量花费就会导致上述征象，而这些又受到神经内分泌的调节。由于涉及碳水化合物、脂质和蛋白质利用的能量代谢相互浸染非常繁芜，这使得阐明这些宏量营养素对能量需求和细胞需求的详细贡献又繁芜化了。
此外，除了影响碳水化合物（葡萄糖）利用、脂质转换（脂肪天生和脂解）、蛋白质引起的产热与脂肪细胞生理的中间代谢通路外，能量平衡还通过繁芜的相互关联的调节过程来坚持，这些调节过程涉及神经内分泌旗子暗记介导的食欲和/或饱足掌握。
常常食用一些单糖，如葡萄糖和果糖，以及摄入饱和脂肪和一些特定的脂肪酸，彷佛是导致肥胖的紧张缘故原由1。伙食纤维的饱腹特性和伙食蛋白质的匆匆饱特性有助于长期干预中的体重坚持和能量摄入掌握。
这种正相互浸染可能是由无脂肪组织和静息代谢的坚持所引起的，但过去 10 年的证据表明，特定的脂肪酸和氨基酸可能参与了肥胖过程，这可能涉及到 FTO 和其它基因的某些多态性100。然而，对付是否存在宏量营养素与 FTO 变异体的相互浸染还没有达成普遍共识109，因此须要进一步研究。
总的来说，目前的证据表明，能量过剩是导致超重和肥胖的紧张缘故原由。假设来自不同宏量营养素的热量相等，那么精制糖和一些脂肪在体重增加中过程中是否存在互补浸染，这仍旧存在争议。
与基因组成和肠道菌群干系的个体特色，可以阐明部分个体间差异：宏量营养素的摄入影响身高体重比和脂肪质量150。事实上，须要进一步的综合研究来理解个体的宏量营养素代谢网络及能量热力学的机制，并根据个体自身的精准营养标准来设计饮食策略。
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原文链接：San-Cristobal R, Navas-Carretero S, Martínez-González M Á, et al. Contribution of macronutrients to obesity: implications for precision nutrition[J]. Nature Reviews Endocrinology, 2020: 1-16.
