Journal
ISCIENCE
Volume 24, Issue 9, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.isci.2021.102963
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Funding
- Ministry of Education, Culture, Sports, Science and Technology (MEXT)
- Japan Society for the Promotion of Science (JSPS) [19K09022]
- Ministry of Health, Labour andWelfare
- Ministry of Agriculture, Forestry and Fisheries
- Japan Diabetes Foundation
- Japan Association for Diabetes Education and Care
- Merck Sharp & Dohme (MSD) Life Science Foundation
- Public Interest Incorporated Foundation
- Suzuken Memorial Foundation
- Grants-in-Aid for Scientific Research [19K09022] Funding Source: KAKEN
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The study demonstrates that medium-chain triglycerides inhibit excessive secretion of GIP from enteroendocrine K cells, leading to reduced obesity and insulin resistance under high long-chain triglyceride diet conditions.
Long-chain triglycerides (LCTs) intake strongly stimulates GIP secretion from enteroendocrine K cells and induces obesity and insulin resistance partly due to GIP hypersecretion. In this study, we found that medium-chain triglycerides (MCTs) inhibit GIP secretion after single LCT ingestion and clarified the mechanism underlying MCT-induced inhibition of GIP secretion. MCTs reduced the CCK effect after single LCT ingestion in wild-type ( WT) mice, and a CCK agonist completely reversed MCT-induced inhibition of GIP secretion. In vitro studies showed that medium-chain fatty acids (MCFAs) inhibit long-chain fatty acid (LCFA)-stimulated CCK secretion and increase in intracellular Ca2+ concentrations through inhibition of GPR120 signaling. Long-term administration of MCTs reduced obesity and insulin resistance in high-LCT diet-fed WT mice, but not in high-LCT diet-fed GIP-knockout mice. Thus, MCT-induced inhibition of GIP hypersecretion reduces obesity and insulin resistance under high-LCT diet feeding condition.
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