Cai_ED_Fig.5.xlsx

Dietary interventions to combat non-communicable diseases focus on optimising food intake but overlook the influence of food structure. Here, we investigate how food structure influences digestion. In a randomised crossover study, ten healthy participants were fitted with nasoenteric tubes that allow simultaneous gastric and duodenal sampling, before consuming iso-nutrient chickpea meals with contrasting cellular structures. Primary outcome is gut hormone response. Secondary outcomes are intestinal content analysis, blood glucose and insulin response, subjective appetite changes and ad libitum energy intake. We show that the ‘broken’ and ‘intact’ cell structures of meals result in different digestive and metabolomic profiles, leading to distinct postprandial gut hormones, glycaemia and satiety responses. ‘Broken' meal structure elicits higher GIP, GLP-1, and blood glycaemia, driven by high starch digestibility and a sharp rise in gastric maltose within 30 minutes. ‘Intact’ meal structure produces a prolonged release of GLP-1 and PYY, elevated duodenal amino acids, and undigested starch at 120 minutes. This work highlights how food structure alters upper gastrointestinal-nutrient-sensing hormones, providing insights into the adverse effects of modern diets on obesity and type 2 diabetes.

旨在对抗非传染性疾病的膳食干预措施，多以优化膳食摄入为核心，却忽视了食物结构的影响。本研究旨在探究食物结构对消化过程的调控作用。本研究采用随机交叉试验设计，招募10名健康受试者，在进食细胞结构存在显著差异的等营养鹰嘴豆餐食前，为其置入可同步采集胃、十二指肠样本的鼻肠管。本研究的主要结局指标为肠道激素应答反应；次要结局指标包括肠道内容物分析、血糖与胰岛素应答反应、主观食欲变化及自由进食能量摄入。研究结果显示，餐食的“破碎”与“完整”细胞结构会带来截然不同的消化过程与代谢组学特征，进而引发具有显著差异的餐后肠道激素应答、血糖水平变化及饱腹感反应。“破碎”餐食结构会引发更高水平的GIP、GLP-1及血糖升高，其机制为高淀粉消化率，以及30分钟内胃内麦芽糖浓度的急剧升高。“完整”餐食结构则会使GLP-1与PYY的释放更为持久，在120分钟时可检测到十二指肠氨基酸水平升高以及未被消化的淀粉残留。本研究揭示了食物结构如何调控上消化道营养感知激素的分泌，为理解现代膳食对肥胖与2型糖尿病的不良影响提供了新的理论视角。