Related Experiment Video
Updated: Sep 11, 2026
DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat
Published on: February 27, 2014
Protective effects of medium-chain triglycerides on the liver and gut in rats administered endotoxin
Hiroshi Kono1, Hideki Fujii, Masami Asakawa
1First Department of Surgery, Yamanashi Medical University, Yamanashi, Japan. hkouno@res.yamanashi-med.ac.jp
Objective:
To determine if medium-chain triglycerides (MCTs) prevent organ injuries and mortality in rats administered endotoxin and to investigate effects of MCT on the gut.
Summary Background Data:
Since dietary MCTs prevent alcohol-induced liver injury by inhibiting activation of Kupffer cells in the enteral feeding model, the authors hypothesized that MCT could prevent deleterious conditions in endotoxemia.
Methods:
After a preliminary experiment determined the optimal dose of MCT, rats were given MCT (5 g/kg per day) or the same dose of corn oil by gavage daily for 1 week. Then, lipopolysaccharide (LPS) was administered intravenously and survival was assessed for the next 24 hours. For analysis of mechanisms, rats were killed 9 hours after LPS injection and serum and liver sections were collected. To investigate effects of MCT on the gut, pathologic change, permeability, and microflora were assessed. Kupffer cells isolated by collagenase digestion and differential centrifugation were used for endotoxin receptor CD14 immunoblotting, phagocytic index, and TNF-alpha production assay.
Results:
All rats given corn oil died after LPS administration; however, this mortality was prevented by MCT in a dose-dependent manner. Rats given corn oil showed liver injury after LPS administration. In contrast, MCT prevented this pathologic change nearly completely. MCT blunted CD14 expression on the Kupffer cells and TNF-alpha production by isolated Kupffer cells; however, there were no differences in phagocytic index between the two groups. The length of the intestinal epithelium was increased in the MCT group compared to the corn oil group. Further, after LPS administration, increases in gut permeability and injury were prevented by MCT. Importantly, MCT also prevented hepatic energy charge and gut injuries in this condition.
Conclusions:
Enteral feeding using MCT could be a practical way of protecting the liver and intestine during endotoxemia.
Insights
Medium-chain triglycerides (MCTs) protect rats from endotoxin-induced mortality and organ damage. This study shows MCTs prevent liver and gut injuries by modulating Kupffer cell activity during endotoxemia.
Area of Science:
- Biochemistry
- Immunology
- Gastroenterology
Background:
- Dietary medium-chain triglycerides (MCTs) are known to prevent alcohol-induced liver injury.
- MCTs achieve this by inhibiting Kupffer cell activation in enteral feeding models.
- This study investigated if MCTs could offer similar protection in endotoxemia.
Purpose of the Study:
- To determine if medium-chain triglycerides (MCTs) prevent organ injuries and mortality in rats exposed to endotoxin.
- To investigate the specific effects of MCTs on the gut during endotoxemia.
Main Methods:
- Rats were gavaged daily with MCTs or corn oil for one week before intravenous lipopolysaccharide (LPS) administration.
- Survival rates were monitored for 24 hours post-LPS.
- Mechanisms were studied by analyzing serum, liver, gut pathology, permeability, microflora, and Kupffer cell function (CD14 expression, phagocytic index, TNF-alpha production).
Main Results:
- MCT administration significantly prevented LPS-induced mortality in a dose-dependent manner.
- MCTs nearly completely prevented liver injury and reduced gut injury and permeability post-LPS.
- MCTs blunted CD14 expression and TNF-alpha production by Kupffer cells but did not affect the phagocytic index.
Conclusions:
- Enteral feeding with medium-chain triglycerides (MCTs) offers significant protection against liver and intestinal injuries during endotoxemia.
- MCTs represent a practical nutritional strategy for mitigating endotoxin-induced organ damage.
