In this article we will discuss about the interactions and metabolic effects of gastro-intestinal hormones.
Interactions of Gastro-Intestinal Hormones:
As gastrin stimulates acid secretion, it probably combines with specific receptor sites on the effector cells. When the concentration of gastrin is high, many receptor sites are occupied and when this concentration is low, few receptor sites are occupied. This relationship between receptor sites and hormones is dynamic. (Figs. 9.33 & 9.39)
Cholecystokinin and gastrin have the competition for binding on the same receptor of the secreting cell due to the presence of same C-terminal sequence in them (active group), so they have same spectrum of activities. One inhibits the other as competitive inhibition of enzymes and the exhibition of the action of hormone will be noted whose concentration is higher than the other.
Gastrin along with cholecystokinin are additive in stimulations of the pancreas and each of these potentiates the stimulating effect of secretion.
Secretin does not possess the same structure as that of gastrin and cannot inhibit histamine-stimulated acid secretion. When secretin exerts its inhibitory activity on acid secretion, it combines with closely related, but different receptor site and hence is non-competitive.
During inhibition of acid secretion and motility by secretin, the pepsinogen secretion is greatly stimulated. Cholecystokinin and secretin does not inhibit pepsinogen secretion.
The inhibitory action of chyme in the duodenum upon acid secretion was attributed to enterogastrone. But when the existence of cholecystokinin (pure) and secretin was proved, much of the action of enterogastrone was observed to be a property of these two hormones.
All the inhibitory activity of acid in the duodenum is the inhibitory action of secretin. A rapid fall in the histamine-stimulated acid secretion is due to the presence of fat in the duodenum, but not the property of cholecystokinin or secretion. Therefore, it may be presumed’ that there is another hormone to be isolated. Moreover, the nervous reflex action mediates some of the inhibitory effects of fat and acid.
Metabolic Effects of Gastro-Intestinal Hormones (Fig. 9.39):
In the gastric and duodenal mucosa of rats it is proved that gastric and pentagastrin stimulate the synthesis of protein. Hyperplasia of the gastric mucosa is the cause of prolonged administration of pentagastrin only in the increased content of parietal cell. Cholecystokinin possesses a similar trophic effect upon the pancreas.
A smaller rise in blood sugar concentration and a prompter increase in plasma insulin content are the effect of glucose absorption from the small intestine than its intravenous administration of an equivalent dosage. Hence this difference proves that there is a role of gastro-intestinal hormones in the metabolic effects. The release of insulin from the p-cells of the islet of Langerhans is stimulated by gastrin, cholecystokinin and secretin and in addition the effect of rising blood glucose concentration in releasing insulin is enhanced by circulating secretin.
Adenyl cyclase activity and lipolysis in the adipose tissue are stimulated by secretin and glucagon due to their similar structure. In these respects, secretin is more potent than glucagon.
