The Procyanidin C1-Dependent Inhibition of the Hydrolysis of Potato Starch and Corn Starch Induced by Pancreatin

Procyanidins are contained in various foods, and their effects on starch hydrolysis have been reported. In Japan, black soybeans, which contain a trimeric procyanidin, procyanidin C1 (proC1), are cooked with rice and used to prepare dumplings. In this study, the effects of proC1 on the pancreatin-induced formation of reducing sugars and starch hydrolysis were studied using potato starch and corn starch. ProC1 inhibited both reactions; the inhibition was greater in potato starch than corn starch when added to heated potato starch and corn starch. When heated with proC1, its inhibitory effects decreased, especially in potato starch, suggesting the important role of proC1 itself for the inhibition of potato starch hydrolysis. ProC1 also inhibited the hydrolysis when added to heated, longer amylose (average molecular weight: 31,200), and the inhibition decreased when heated with the amylose. On the other hand, proC1 could not inhibit the hydrolysis when added to heated, shorter amylose (average molecular weight: 4500), but could when heated with the amylose, suggesting the important role of the degradation products of proC1 for the inhibition. We discuss the mechanism of the proC1-dependent inhibition of amylose hydrolysis, taking the molecular weight into account

Possible Reactions of Dietary Phenolic Compounds with Salivary Nitrite and Thiocyanate in the Stomach

Foods are mixed with saliva in the oral cavity and swallowed. While staying in the stomach, saliva is contentiously provided to mix with the ingested foods. Because a salivary component of nitrite is protonated to produce active nitrous acid at acidic pH, the redox reactions of nitrous acid with phenolic compounds in foods become possible in the stomach. In the reactions, nitrous acid is reduced to nitric oxide (•NO), producing various products from phenolic compounds. In the products, stable hydroxybezoyl benzofuranone derivatives, which are produced from quercetin and its 7-O-glucoside, are included. Caffeic acid, chlorogenic acid, and rutin are oxidized to quinones and the quinones can react with thiocyanic acid derived from saliva, producing stable oxathiolone derivatives. 6,8-Dinitrosocatechis are produced from catechins by the redox reaction, and the dinitrocatechins are oxidized further by nitrous acid producing the quinones, which can make charge transfer complexes with the dinitrosocatechin and can react with thiocyanic acid producing the stable thiocyanate conjugates. In this way, various products can be produced by the reactions of salivary nitrite with dietary phenolic compounds, and reactive and toxic quinones formed by the reactions are postulated to be removed in the stomach by thiocyanic acid derived from saliva

Suppression of Pancreatin-Induced Digestion of Starch in Starch Granules by Starch/Fatty Acid and Starch/Flavonoid Complexes in Retrograding Rice Flour

Adzuki beans are used to prepare foods with glutinous and non-glutinous rice in Japan, and adzuki bean pigments are able to color rice starch a purplish red. This study deals with the adzuki bean extract-dependent suppression of starch digestion of non-glutinous rice flour (joshinko in Japanese), which was gelatinized in boiling water and then cooled to 37 °C. Accompanying the treatment of joshinko with pancreatin, amylose and amylopectin were released from the joshinko particles, and the released amylose and amylopectin were further digested. The adzuki extract suppressed the release and digestion by binding to amylose and amylopectin, which were present in the particles and at the surfaces of the particles. Fatty acids and flavonoids in the adzuki extract contributed to the suppression. In addition, the starch digestion in the joshinko particles appeared to be suppressed if the amylose/fatty acid complexes and amylose/flavonoid and amylopectin/flavonoid complexes, which are poor substrates of α-amylase, surrounded the particles. It is discussed that the suppression was due to the prevention of α-amylase access to the particles