RYGB alters intestinal lipid metabolism and increases portal levels of anti-diabetic phospholipids
Tammy Lo, Renuka Subramaniam, Eric Sheu, Ali Tavakkoli
Brigham and Women's Hospital, Boston, MA, USA
Background: Roux-en-Y gastric bypass (RYGB) leads to intestinal hypertrophy and hyperplasia. We hypothesized that RYGB alters enterocyte lipid handling to support this increased bioenergetic demand. The subsequent release of novel lipid metabolites within the portal milieu send signals to the liver which mediates insulin sensitivity.
Methods: RYGB or sham surgeries were performed in diet-induced obese and insulin resistant rats. Biliopancreatic, Roux, and common limb in RYGB rats with their respective counterparts in sham were harvested after fasting or feeding. qPCR was performed to determine intestinal mRNA expression levels of fatty acid (FA) uptake transporters and FA β-oxidation proteins. Portal lipid metabolites were characterized using liquid chromatography coupled to mass spectrometry.
Results: At fasting, there was downregulation of FA uptake transporters and FA β-oxidation in enterocytes, with lowering of portal diglyceride and triglyceride levels. Portal long-chain phospholipids (phosphatidylcholine) were however increased. After feeding, there was a significant increase in gene expression for FA uptake and FA β-oxidation (table 1).
Conclusion: RYGB induces metabolic changes in enterocytes. During fed state, there is an increase in enterocyte lipid metabolism which leads to unique changes in portal milieu. As long chain phospholipids are known to promote insulin sensitivity, these changes may be responsible for the rapid improvement in diabetes after RYGB.
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