Cholecystokinin does not mediate glucose's cytoprotective effects.

Area of Science:

• Gastroenterology
• Physiology
• Pharmacology

Background:

• Cold restraint stress causes acute gastric mucosal injury.
• Enteral nutrients, like glucose, prevent this injury by inhibiting gastric emptying.
• Cholecystokinin (CCK) is released by nutrients and may inhibit gastric emptying, suggesting a potential role in cytoprotection.

Purpose of the Study:

• To investigate if cholecystokinin (CCK) mediates the gastric mucosal protection observed with enteral nutrients during cold restraint stress.
• To determine the role of CCK in the physiological changes induced by enteral glucose under stress conditions.

Main Methods:

• Three experiments were conducted to assess the effects of CCK and CCK receptor antagonism (using L-364,718) on gastric mucosal injury during cold restraint stress.
• Measurements included gastric mucosal protection, gastric volume, pH, and mucin content.
• Evaluated the impact of exogenous CCK on glucose-induced physiological changes.

Main Results:

• Enteral glucose demonstrated significant gastric mucosal protection, increasing gastric volume, luminal pH, and mucin.
• Neither physiological nor pharmacological doses of CCK provided mucosal protection.
• Exogenous CCK did not affect glucose-induced changes in gastric function.
• CCK receptor antagonism did not alter protection or have independent effects.

Conclusions:

• Enteral glucose protects the gastric mucosa from cold restraint injury through beneficial effects on gastric physiology.
• The protective mechanisms of enteral glucose in this model are independent of cholecystokinin (CCK).