Glycemic carbohydrates in foods are an important macronutrient providing the biological fuel of glucose for a variety of physiological processes. A classification of glycemic carbohydrates into rapidly digestible carbohydrate (RDC) and slowly digestible carbohydrate (SDC) has been used to specify their nutritional quality related to glucose homeostasis that is essential to normal functioning of the brain and critical to life. Although there have been many studies and reviews on slowly digestible starch (SDS) and SDC, the mechanisms of their slow digestion and absorption were mostly investigated from the material side without considering the physiological processes of their in vivo digestion, absorption, and most importantly interactions with other food components and the gastrointestinal tract. In this article, the physiological processes modulating the bioavailability of carbohydrates, specifically the rate and extent of their digestion and absorption as well as the related locations, in a whole food context, will be discussed by focusing on the activities of the gastrointestinal tract including glycolytic enzymes and glucose release, sugar sensing, gut hormones, and neurohormonal negative feedback mechanisms. It is hoped that a deep understanding of these physiological processes will facilitate the development of innovative dietary approaches to achieve desired carbohydrate or glucose bioavailability for improved health.

Dysregulated glucose metabolism is associated with many chronic diseases such as obesity and type 2 diabetes mellitus (T2DM), and strategies to restore and maintain glucose homeostasis are essential to health. The incretin hormone of glucagon‐like peptide‐1 (GLP‐1) is known to play a critical role in regulating glucose homeostasis and dietary nutrients are the primary stimuli to the release of intestinal GLP‐1. However, the GLP‐1 producing enteroendocrine L‐cells are mainly distributed in the distal region of the gastrointestinal tract where there are almost no nutrients to stimulate the secretion of GLP‐1 under normal situations. Thus, a dietary strategy to sustain the release of GLP‐1 was proposed, and the slow digestion property and dipeptidyl peptidase IV (DPP‐IV) inhibitory activity of food components, approaches to reduce the rate of food digestion, and mechanisms to sustain the release of GLP‐1 were reviewed. A slow digestion‐oriented dietary approach through encapsulation of nutrients, incorporation of viscous dietary fibers, and enzyme inhibitors of phytochemicals in a designed whole food matrix will be implemented to efficiently reduce the digestion rate of food nutrients, potentiate their distal deposition and a sustained secretion of GLP‐1, which will be beneficial to improved glucose homeostasis and health.

The effect of tea polyphenols (TPL) on the gluten network structure in TPL-fortified bread and dough systems was investigated. In the bread system, the addition of tea polyphenols (TPL) dose-dependently (0, 0.5, 1.0, 1.5, and 2%) deteriorated the bread quality in terms of the loaf volume, hardness and sensory properties. In the gluten dough system (2% TPL), farinograph results showed that the stability and development time of the bread dough were decreased, resulting in a weak dough with a significantly increased elastic modulus (G′). The disulfide bonds, key to the dough network formation, were decreased by 9.9 μmol g⁻¹ (24.2%), and their stability was also reduced due to the reduction (15.0%) of the relative content of the gauche–gauche–gauche structure. The addition of tea polyphenols also increased the internal hydrogen bonds and hydrophobic forces along with the increased random coil and decreased α-helix secondary structure of gluten. The water distribution experiment showed that the bound water peak in the nuclear magnetic resonance (NMR) spectrum disappeared, but the adsorbed water and free water were increased by 17.3% and 0.4%, respectively. Collectively, the interaction between wheat gluten and tea polyphenols affects the water–gluten relationship and the protein structure, which leads to a disrupted network structure of the wheat dough and deteriorated bread quality. Strategies to prevent gluten–phenolic interaction in functional bread preparation warrant further investigation.