No abstract

The widespread application of TiO2 nanoparticles (NPs) as additives in foods such as gum, candy and puddings has dramatically increased the human ingestion and accumulation of these nanomaterials. Although the toxicity of TiO2 NPs has been extensively studied, their impact on gut microbiota in vivo still needs further research. In this study, TiO2 NPs with two main crystalline phases anatase and rutile were orally administrated to mice for 28 days. The dynamic influences of anatase and rutile on gut microbiota structures were investigated at doses equivalent to those consumed by people who love to eat candies. The results showed that titanium accumulated in the spleen, lung, and kidney but had no significant effects on organ histology. Gavage of rutile NPs but not anatase NPs resulted in longer intestinal villi and irregular arrangement of villus epithelial cells. Treatment with TiO2 NPs did not decrease gut microbiota diversity but shifted their structures in a time-dependent manner. Rutile NPs had a more pronounced influence on the gut microbiota than anatase NPs. The most influenced phylum was Proteobacteria, which was significantly increased by rutile but not by anatase. At the genus level, Prevotella was significantly decreased by both the TiO2 NPs, Rhodococcus was enriched by rutile NPs, and Bacteroides was increased by anatase NPs. Overall, these results suggested that chronic overconsumption of TiO2 NP-containing foods is likely to deteriorate the gastrointestinal tract and change the structures of microbiota. The crystalline phases may play an important role in mediating the intestinal impact of TiO2 NPs.

Hyperlipidemia is considered to be one of the greatest risk factors contributing to the prevalence and severity of cardiovascular diseases. In this work, we investigated the anti-hyperlipidemic effect and potential mechanism of action of the Pandanus tectorius fruit extract in hamsters fed a high fat-diet (HFD). The n-butanol fraction of the P. tectorius fruit ethanol extract (PTF-b) was rich in caffeoylquinic acids (CQAs). Administration of PTF-b for 4 weeks effectively decreased retroperitoneal fat and the serum levels of total cholesterol (TC), triglycerides (TG) and low density lipoprotein–cholesterol (LDL-c) and hepatic TC and TG. The lipid signals (fatty acids, and cholesterol) in the liver as determined by nuclear magnetic resonance (NMR) were correspondingly reduced. Realtime quantitative PCR showed that the mRNA levels of PPARα and PPARα-regulated genes such as ACO, CPT1, LPL and HSL were largely enhanced by PTF-b. The transcription of LDLR, CYP7A1, and PPARγ was also upregulated. Treatment with PTF-b significantly stimulated the activation of AMP-activated protein kinase (AMPK) as well as the activity of serum and hepatic lipoprotein lipase (LPL). Together, these results suggest that administration of the PTF-b enriched in CQAs moderates hyperlipidemia and improves the liver lipid profile. These effects may be caused, at least in part, by increasing the expression of PPARα and its downstream genes and by upregulation of LPL and AMPK activities.