The acute effect of a β-glucan-enriched oat bread on gastric emptying, GLP-1 response, and postprandial glycaemia and insulinemia: a randomised crossover trial in healthy adults

IF 3.9 2区医学 Q2 NUTRITION & DIETETICS

Nutrition & Metabolism Pub Date : 2024-03-18 DOI:10.1186/s12986-024-00789-w

Ingrid Revheim, Simon Ballance, Adelheid Fretland Standal, Anne Rieder, Jutta Dierkes, Anette E. Buyken, Odd Helge Gilja, Trygve Hausken, Hanne Rosendahl-Riise

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引用次数: 0

Abstract

The cereal fibre β-glucan reduces postprandial glycaemia, however, the underlying mechanisms are not fully understood. Thus, the aim of this study was to investigate the acute effect of a β-glucan-enriched oat bread on gastric emptying half-time (T1/2), gastric emptying lag phase (Tlag), and gastric emptying rate (GER), and the secretion of glucagon-like peptide-1 (GLP-1) as potential means to influence postprandial glycaemia. A randomised crossover trial was conducted in 22 healthy adults (age 24.6 ± 3.1 years, BMI 23.1 ± 2.7 kg/m2) receiving 25 g available carbohydrates from a β-glucan-enriched oat bread or a control whole-wheat bread at two non-consecutive days. T1/2, Tlag, and GER were determined based on ultrasound measures of the cross-sectional gastric antrum area in the fasting state and 15, 30, 45, 60, 90, and 120 min postprandially. Capillary glucose, serum insulin, and plasma GLP-1 concentrations were measured at the same time points. A biphasic pattern of gastric emptying with a distinct Tlag before the commencement of emptying was observed in most subjects for both bread types. While no differences in GER were evident (p = 0.562), consumption of the oat bread significantly increased T1/2 by 18 min and Tlag by 14 min compared with the whole-wheat bread (p = 0.005 and p = 0.010, respectively). In addition, the oat bread significantly reduced iAUC2h for glucose and insulin responses compared with the whole-wheat bread (p = 0.001 and p < 0.001, respectively). There were no significant differences in GLP-1 response between the two breads (p = 0.892). The increased T1/2 and Tlag could offer a potential mechanism for the observed attenuation of postprandial glycaemia and insulinemia after consumption of the β-glucan-enriched oat bread compared with the whole-wheat bread. Trial registration: The study is registered at clinicaltrails.gov (NCT04571866).

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富含β-葡聚糖的燕麦面包对胃排空、GLP-1 反应以及餐后血糖和胰岛素血症的急性影响：一项针对健康成年人的随机交叉试验

谷物纤维β-葡聚糖可降低餐后糖血症，但其潜在机制尚不完全清楚。因此，本研究旨在调查富含β-葡聚糖的燕麦面包对胃排空半衰期（T1/2）、胃排空滞后期（Tlag）、胃排空率（GER）和胰高血糖素样肽-1（GLP-1）分泌的急性影响，以此作为影响餐后血糖的潜在手段。我们对 22 名健康成年人（年龄为 24.6 ± 3.1 岁，体重指数为 23.1 ± 2.7 kg/m2）进行了随机交叉试验，让他们在非连续的两天内从富含β-葡聚糖的燕麦面包或对照全麦面包中摄入 25 克可用碳水化合物。T1/2、Tlag 和 GER 是根据空腹状态和餐后 15、30、45、60、90 和 120 分钟胃窦横截面积的超声测量结果确定的。毛细血管葡萄糖、血清胰岛素和血浆 GLP-1 浓度也在同一时间点测定。在两种面包中，大多数受试者的胃排空呈双相模式，在开始排空前有一个明显的Tlag。虽然胃排空率没有明显差异（p = 0.562），但与全麦面包相比，燕麦面包的 T1/2 显著增加了 18 分钟，Tlag 显著增加了 14 分钟（分别为 p = 0.005 和 p = 0.010）。此外，与全麦面包相比，燕麦面包明显降低了葡萄糖和胰岛素反应的 iAUC2h（分别为 p = 0.001 和 p < 0.001）。两种面包的 GLP-1 反应无明显差异（p = 0.892）。与全麦面包相比，食用富含β-葡聚糖的燕麦面包后，T1/2和Tlag的增加可能是观察到的餐后血糖和胰岛素血症减轻的潜在机制。试验注册：该研究已在 clinicaltrails.gov 注册（NCT04571866）。

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来源期刊

Nutrition & Metabolism 医学-营养学

CiteScore

8.40

自引率

0.00%

发文量

审稿时长

4-8 weeks

期刊介绍： Nutrition & Metabolism publishes studies with a clear focus on nutrition and metabolism with applications ranging from nutrition needs, exercise physiology, clinical and population studies, as well as the underlying mechanisms in these aspects. The areas of interest for Nutrition & Metabolism encompass studies in molecular nutrition in the context of obesity, diabetes, lipedemias, metabolic syndrome and exercise physiology. Manuscripts related to molecular, cellular and human metabolism, nutrient sensing and nutrient–gene interactions are also in interest, as are submissions that have employed new and innovative strategies like metabolomics/lipidomics or other omic-based biomarkers to predict nutritional status and metabolic diseases. Key areas we wish to encourage submissions from include: -how diet and specific nutrients interact with genes, proteins or metabolites to influence metabolic phenotypes and disease outcomes; -the role of epigenetic factors and the microbiome in the pathogenesis of metabolic diseases and their influence on metabolic responses to diet and food components; -how diet and other environmental factors affect epigenetics and microbiota; the extent to which genetic and nongenetic factors modify personal metabolic responses to diet and food compositions and the mechanisms involved; -how specific biologic networks and nutrient sensing mechanisms attribute to metabolic variability.