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Published on: July 21, 2017
The importance of triglyceride hydrolysis for the release of gastric inhibitory polypeptide
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.
Abstract:
Gastric inhibitory polypeptide is released from the small intestine after the ingestion of fat, but it is not known if triglyceride itself or one of its hydrolytic products is the stimulus to gastric inhibitory polypeptide secretion. Children with cystic fibrosis and defective fat lipolysis were studied to help define the exact stimulus to gastric inhibitory polypeptide secretion. Pancreatic enzyme therapy was withheld from the children with cystic fibrosis during these tests. Ten normal children and 10 children with cystic fibrosis each ingested corn oil and serum immunoreactive gastric inhibitory polypeptide measured. The normal children had a 10-fold increase in serum gastric inhibitory polypeptide levels after the triglyceride, but no increase in immunoreactive gastric inhibitory polypeptide occurred in the children with cystic fibrosis. When three of the children with cystic fibrosis received their pancreatic enzymes and then ingested the triglyceride, gastric inhibitory polypeptide values increased 10-fold. To assess the relative importance of the products of triglyceride hydrolysis and the chain length of the component fatty acids, 6 normal adults consumed, on separate days, 40 mmol of corn oil, medium-chain triglycerides, long-chain fatty acids, or glycerol. Long-chain fatty acids caused a fourfold increase and triglyceride a 12-fold increase in gastric inhibitory polypeptide levels. There was no increase after medium-chain triglyceride or glycerol. This indicates that long-chain fatty acids-the end product of triglyceride hydrolysis-are a stimulus to gastric inhibitory polypeptide secretion; that this release is apparently proportional to the quanitity of long-chain fatty acid present; and that hydrolysis of triglyceride is required before gastric inhibitory polypeptide release can normally occur after fat ingestion.
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