No abstract

The effect of salivary amylase on changes in gastric protein hydrolysis was studied. The study was carried out in vitro, saliva, gastric juice, solutions of starch, casein, albumin and hemoglobin were used in the work. It was concluded that the use of starch-protein mixtures helps to reduce protein hydrolysis by gastric juice, due to the formation of starch-protein complexes that prevent protein hydrolysis, and reduce the access of gastric proteases to proteins in the starch-protein complex. An increase in the ratio of starch and protein in the direction of increasing starch contributes to an additional decrease in protein hydrolysis, which may be an additional decrease in the access of gastric proteases to proteins, in addition to an obstacle to proteins in the starch-protein complex. In addition, salivary amylase helps to improve the digestibility of proteins by gastric juice, both due to a decrease in starch-protein complexes, and to increase the access of proteases to proteins by reducing the concentration of starch as a result of its digestion by salivary amylase.

The effect of various concentrations of fat hydrolysis products on the pancreatic and gastric juices OPA using casein-fat emulsion (casein + tributyrin, casein + sunflower oil) was studied. It is concluded that the hydrolysis products of sunflower oil, contributes to a significant decrease in pancreatic juice OPA, which are less pronounced under the influence of tributyrin hydrolysis products.The hydrolysis products of both sunflower oil and tributyrinare less pronounced in an acidic environment to reduce the gastric juice OPA. An increase in the concentration of both sunflower oil and tributyrin in the emulsion with casein contributes to a significant increase in pancreatic juice OPA. At the same time, the effect of tributyrinis less pronounced than when using sunflower oil. At the same time, an increase in the concentration of both tributyrin and sunflower oil to a lesser extent affects the increase in the gastric juice gastric arteries.

No abstract

The aim of the study was to examine specifics of changes in the level of stomach- and pancreas-released blood hydrolases in chronic viral hepatitis B and analyze the mechanisms underlying such changes. We assessed serum markers of HBV infection, liver enzymes tests as well as gastric and pancreatic hydrolase level. The patients examined were divided into three groups: control (healthy) and two study groups — HBV post-infection and chronic HBV infection. Patients with HBV post-infection had no significant deviations from normal range for blood level of gastric and pancreatic hydrolases. Patients with chronic HBV infection were found to contain increased blood level of amylase and lipase, which may evidence about increasing pancreatic functional activity and development of covert pancreatitis. At the same time, decline in the concentration of serum pepsinogen-1 below 40 μg/l could indicate about prominently decreased secretion of hydrochloric acid and development of atrophic gastritis, and it was found that the major factor contributing to development of such disorders was the short-chain peptide CCK-8, which utilization declines in patients with chronic HBV infection. CCK-8 can play a pivotal role in inhibiting stimulation of gastric acid secretion and controls gastric acid, plasma gastrin and somatostatin secretion. Cholecystokinin has been found to inhibit acid secretion by activating CCK type A receptors as well as via somatostatin-involving mechanism. The secretion of gastric somatostatin-14 increased by fivefold due to CCK-8 alone, but was blocked by the CCK-A receptor blocker loxiglumide. These data show that CCK-8 directly inhibits acid reactions by stimulating the release of gastric somatostatin indirectly through the CCK-A receptor. Thus, it can be assumed that normally CCK-8 is mainly utilized by the liver, which is altered during chronic hepatitis B resulting in elevated blood CCK-8 concentration. As a consequence, it enhances pancreatic secretion resulting in developing pancreatitis that is paralleled with inhibited gastric secretion and emerged atrophic gastritis.