Summary
Previous study from our laboratory demonstrated that an increased release of gut glucagon-like
immunoreactivity (GLI) following triglyceride digestion was not observed in pancreatectomized
dogs. Therefore, in order to clarify the response of gut GLI to triglyceride ingestion,
experimental study was carried out in normal and pancreatectomized dogs. When butter
was administered to pancreatectomized dogs in combination with pancreatic enzymes,
plasma glucagon (IRG) measured by specific antiserum did not change significantly
but plasma triglyceride as well as plasma total immunoreactive glucagon (total IRG)
measured by nonspecific antiserum increased. Oral administration of glycerol induced
no significant increase in plasma IRG but elicited a moderate increase of plasma total
IRG. Gastric instillation of palmitic acid induced a remarkable rise of plasma total
IRG in normal dogs, whereas plasma IRG did not reveal any changes. Oral administration
of triglyceride of medium chain fatty acid, tricaprylin, did not promote any rise
of plasma IRG but a slight increase of plasma total IRG. From the present experiment,
it is concluded that hydrolysis of triglyceride and its metabolites are important
in the release of gut GLI following fat ingestion. Among its metabolites, long chain
fatty acid and glycerol promote the GLI secretion, whereas medium chain fatty acid
does not.
Key-Words:
Glucagon-Like Immunoreactivity (GLI)
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Pancreatic Enzyme
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Glycerol
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Palmitate
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Tricaprylin
