Abstract
Triacylglycerol (TG) is categorized into long-, medium-, and short-chain TG (SCTG). While the digestion of long- and medium-chain TG is well established, the process for SCTG remains unclear. This study investigated SCTG digestion by administering 2 mmol of triacetin to rats and analyzing acetin, acetic acid, and glycerol levels in the portal blood and small intestine. Triacetin was fully degraded in the upper gastrointestinal tract and absorbed as acetic acid and glycerol. Glycerol influx into the liver promoted gluconeogenesis, while acetate activated AMPK, resulting in the suppression of fatty acid synthesis-related genes and the upregulation of fatty acid β-oxidation-related genes. These findings demonstrate that triacetin not only serves as a substrate for energy metabolism but also regulates hepatic gene expression, highlighting its dual role as both a metabolic substrate and signaling molecule. Triacetin thus shows potential as a dietary modulator for improving metabolic health.
Published Version
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