Acetyl-L-carnitine attenuates Poly I:C-induced sickness behavior in mice.

Fatigue is accompanied by a decrease in physical activity or malaise, and might be reduced by acetyl-L-carnitine (ALC) administration. The purpose of this study was to investigate the preventive effects of ALC on Poly I:C-induced sickness behavior in mice. For the experiment, male C3H/HeN mice were used and treated with ALC for 5 days before Poly I:C administration. ALC administration attenuated the decrease in wheel behavior activity of mice at 24 h after Poly I:C administration and ALC-treated mice quickly recovered from the sickness behavior. The gene expression of brain-derived neurotrophic factor (BDNF) in the cerebrum and hippocampus, which is associated with physical activity, was higher in the ALC-treated group. Translocator protein 18kDa (TSPO), which has cytoprotective effects, was up-regulated in the cerebrum and hippocampus, suggesting that ALC suppressed the decrease in activity induced by Poly I:C treatment through enhancement of cytoprotective effects in the brain.

LPS-induced TNF-α production is attenuated by intake with PHGG via gut microbial fermentation in mice.

OBJECTIVES: Intake of dietary fibers promotes the production of short-chain fatty acids (SCFAs), which can affect host inflammation via gut microbial fermentation. Although partially hydrolyzed guar-gum (PHGG) is a water-soluble dietary fiber with lower viscosity, its benefits in acute inflammation are yet to be determined. The aim of this study was to investigate the effect of PHGG intake on the lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-α production. METHODS: Nine-wk-old male C3 H/HeN mice were used in this study, and they were randomly divided into control diet (CD) and CD + 5% PHGG (GGCD) groups. After a dietary intervention of 6 wk, LPS (1 mg/kg) was injected into the orbital vein. Plasma TNF-α concentration and SCFAs in cecum contents were then measured. Also, the effect of gut microbiota on LPS-induced TNF-α production was evaluated in PHGG-fed mice before and after antibiotic treatment. RESULTS: PHGG intake accelerated a dramatic suppression of LPS-induced TNF-α production (P < 0.01). PHGG-induced low pH in feces (P < 0.05) indicates that the gut microbiota induced high fermentation. Indeed, SCFAs in cecum contents of GGCD mice were significantly higher than in the CD group (P < 0.05). Furthermore, PHGG intake after antibiotic treatment did not induce the suppression of TNF-α. CONCLUSION: These results demonstrated that inflammation was inhibited by habitual PHGG ingestion, suggesting that this phenomenon might be associated with changes in gut microbiota-induced SCFAs production.

The Effect of Voluntary Exercise on Gut Microbiota in Partially Hydrolyzed Guar Gum Intake Mice under High-Fat Diet Feeding.

Although dietary fiber treatment alters the gut microbiota and its metabolite production, it is unclear whether or not exercise habits can have a supplemental effect on changes in gut microbiota in dietary fiber-treated mice. To clarify the supplemental effect of voluntary exercise on gut microbiota in partially hydrolyzed guar gum (PHGG), which is a soluble dietary fiber, treated mice under high-fat diet (HFD) feeding, 4-week-old male C57BL/6J mice (n = 80) were randomly divided into two dietary groups: the control-diet (CD) and HFD. Then, each dietary group was treated with or without PHGG, and with or without wheel running. After the experimental period, measurement of maximal oxygen consumption, a glucose tolerance test and fecal materials collection for analysis of gut microbiota were carried out. Voluntary exercise load in PHGG treatment under HFD feeding showed the supplemental effect of exercise on obesity (p < 0.01) and glucose tolerance (p < 0.01). Additionally, in both CD and HFD groups, voluntary exercise accelerated the decrease in the Firmicutes/Bacteroidetes ratio in mice fed with PHGG (p < 0.01). These findings suggest that voluntary exercise might activate the prevention of obesity and insulin resistance more via change in gut microbiota in mice administrated with PHGG.