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Oral tributyrin prevents endotoxin-induced lipid metabolism disorder
- Miyoshi, Makoto, Iizuka, Norihito, Sakai, Shota, Fujiwara, Mayu, Aoyama-Ishikawa, Michiko, Maeshige, Noriaki, Hamada, Yasuhiro, Takahashi, Michiko, Usami, Makoto
- Clinical nutrition ESPEN 2015 v.10 no.2 pp. e83
- Western blotting, acetylation, beta oxidation, blood lipids, dairy products, enzymes, fatty acid metabolism, fatty acid-binding proteins, fatty acids, histones, hormone receptors, laboratory animals, lipid metabolism disorders, lipopolysaccharides, liver, low density lipoprotein cholesterol, oral administration, peroxisome proliferator-activated receptors, protective effect, protein metabolism, quantitative polymerase chain reaction, rats, transcription factor NF-kappa B, transport proteins, triacylglycerols, tributyrin
- Sepsis leads to dysregulation of lipid and lipoprotein metabolism. Butyrate increases peroxisome proliferator-activated receptors (PPARs), which are key nuclear hormone receptors to induce fatty acid oxidation and synthesis. Oral administration of tributyrin, a prodrug of butyrate contained in dairy products, suppresses lipopolysaccharide (LPS)-induced liver injury through attenuating nuclear factor-κB activity with an increased hepatoportal butyrate level. In this study, we elucidated the protective effect of oral administration of tributyrin against LPS-mediated lipid metabolism disorder in rats.Male Wistar rats were randomly divided and were administered tributyrin or vehicle orally 1 h before LPS injection and then sacrificed at 0, 1.5, 6, and 24 h after LPS. Liver tissue expressions of nuclear hormone receptors, enzymes associated with fatty acid metabolism, and histone acetylation were analyzed by real-time polymerase chain reaction or western blotting. Plasma lipids levels were measured.Tributyrin enhanced expression of PPARs and histone H3 in the liver at basal levels. Tributyrin suppressed LPS-induced repression of PPARs fatty acid oxidation-associated enzymes: fatty acid transport protein and fatty acid binding protein, and fatty acid synthesis-associated enzyme: sterol regulatory element binding protein-1c. Tributyrin reduced the increase in plasma triglyceride, total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) levels at 24 h after LPS injection.Oral tributyrin administration prevented elevation of plasma triglyceride, TC, and LDL-C levels through improved fatty acid oxidation in endotoxemic rats.