The importance of triglyceride hydrolysis for the release of gastric inhibitory polypeptide

Gastroenterology
|January 1, 1981
PubMed

Insights

Long-chain fatty acids, a product of triglyceride digestion, stimulate gastric inhibitory polypeptide (GIP) secretion. This process requires triglyceride hydrolysis, as shown in studies with cystic fibrosis patients and normal individuals.

Area of Science:

  • Gastroenterology
  • Endocrinology
  • Metabolic Research

Background:

  • Gastric inhibitory polypeptide (GIP) release from the small intestine follows fat ingestion.
  • The precise stimulus for GIP secretion—triglyceride itself or its hydrolysis products—remains unclear.

Purpose of the Study:

  • To identify the specific stimulus for gastric inhibitory polypeptide secretion after fat ingestion.
  • To investigate the role of triglyceride hydrolysis products in GIP release.

Main Methods:

  • Studied children with cystic fibrosis (impaired fat digestion) and normal children, measuring serum GIP after corn oil ingestion without pancreatic enzymes.
  • Administered pancreatic enzymes to cystic fibrosis patients before triglyceride ingestion.
  • In normal adults, assessed GIP response to corn oil, medium-chain triglycerides, long-chain fatty acids, and glycerol.

Main Results:

  • Normal children showed a 10-fold GIP increase after triglyceride; cystic fibrosis patients showed no increase without enzymes.
  • Cystic fibrosis patients exhibited a 10-fold GIP increase when given pancreatic enzymes prior to triglyceride.
  • Long-chain fatty acids induced a fourfold GIP increase, while triglyceride caused a 12-fold increase in normal adults; medium-chain triglycerides and glycerol did not stimulate GIP.

Conclusions:

  • Long-chain fatty acids, the end product of triglyceride hydrolysis, are a primary stimulus for GIP secretion.
  • GIP release is proportional to the amount of long-chain fatty acid available.
  • Triglyceride hydrolysis is a necessary step for normal GIP release following fat ingestion.

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