Pepsinogens are secreted in a form such that the activation peptide assumes a compact structure that occludes the active site. On exposure to an acidic pH the activation peptide is cleaved, thereby unmasking the active site and generating catalytically-active pepsin. Optimal activity of pepsins is at pH of 1. They are reversibly inactivated at about pH 5 and irreversibly inactivated at pH 7 to 8.
In general, secretion of pepsinogens is coupled to secretion of acid from the parietal cell. In vitro studies have demonstrated that secretion is effectively stimulated by agents that stimulate either of two conditions:. Receptors for many of the hormones listed above have been demonstrated on chief cells and pepsinogen secretion has been stimulated or blocked by exposure to these agents or their antagonists, respectively.
At the present time it seems safe to say that the principal physiologic secretagogue s regulating pepsinogen secretion has not been clearly deliniated.
The activation of protein kinase C PK-C would appear to be involved in regulatory processes. The measurement of pepsinogens A and C in the serum is considered to be one of the non-invasive biochemical markers for monitoring peptic secretion and obtaining information on the gastric mucosa status of healthy subjects. Recently, pepsinogen measurements have been used as an effective biochemical method for evaluating and monitoring patients with gastrointestinal diseases and for checking the effects of drug treatment.
The level of PGA in the serum is always high in normal gastritis, while in atrophic gastritis it is always low. In both cases the PGC level in the serum is high. It has been suggested that the origin of the gastrointestinal distress experienced by long distance runners is a transient ischaemia of the gastric mucosa; it is also suggested that a hypobaric-hypoxic environment could contribute to induce gastric mucosa necrosis.
Interrelation between gastrointestinal distress, hypobaric-hypoxic environment and modifications of PGA and PGC, gastrin and cortisol was evaluated in 13 athletes after a marathon performed at m.
No relationship was observed between gastrointestinal symptoms and hormonal changes after the race. A control group of five subjects, who had been exposed to the same environmental conditions, showed no gastrointestinal or hormonal alteration.
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