Strawberry (Fragaria chiloensis) is a major edible berry with various potential health benefits. This study determined the protective effects of whole strawberry (WS) against dextran-sulfate-sodium-induced colitis in mice. In colitic mice, dietary WS reduced the disease activity index, prevented the colon shortening and spleen enlargement, and alleviated the colonic tissue damages. The abundance of proinflammatory immune cells was reduced by dietary WS in the colonic mucosa, which was accompanied by the suppression of overproduction of proinflammatory cytokines. Western blotting and immunohistochemical analysis revealed that dietary WS decreased the expression of proinflammatory proteins in the colonic mucosa. Moreover, dietary WS partially reversed the alteration of gut microbiota in the colitic mice by increasing the abundance of potential beneficial bacteria, e.g., Bifidobacterium and Lactobacillus, and decreasing the abundance of potential harmful bacteria, e.g., Dorea and Bilophila. Dietary WS also restored the decreased production of short-chain fatty acids in the cecum of the colitic mice. The results revealed the anti-inflammatory effects and mechanisms of dietary WS in the colon, which is critical for the rational utilization of strawberry for the prevention of inflammation-driven diseases.

The recent ban of titanium dioxide (TiO2) as a food additive (E171) in France intensified the controversy on safety of foodborne‐TiO2 nanoparticles (NPs). This study determines the biological effects of TiO2 NPs and TiO2 (E171) in obese and non‐obese mice. Oral consumption (0.1 wt% in diet for 8 weeks) of TiO2 (E171, 112 nm) and TiO2 NPs (33 nm) does not cause severe toxicity in mice, but significantly alters composition of gut microbiota, for example, increased abundance of Firmicutes phylum and decreased abundance of Bacteroidetes phylum and Bifidobacterium and Lactobacillus genera, which are accompanied by decreased cecal levels of short‐chain fatty acids. Both TiO2 (E171) and TiO2 NPs increase abundance of pro‐inflammatory immune cells and cytokines in the colonic mucosa, indicating an inflammatory state. Importantly, TiO2 NPs cause stronger colonic inflammation than TiO2 (E171), and obese mice are more susceptible to the effects. A microbiota transplant study demonstrates that altered fecal microbiota by TiO2 NPs directly mediate inflammatory responses in the mouse colon. Furthermore, proteomic analysis shows that TiO2 NPs cause more alterations in multiple pathways in the liver and colon of obese mice than non‐obese mice. This study provides important information on the health effects of foodborne inorganic nanoparticles.

Polymethoxyflavones (PMFs) have been shown to prevent obesity, ameliorate type 2 diabetes, and regulate lipid metabolism in vitro and in vivo. However, little is known about the contribution of 3,5,6,7,8,3′,4′-heptamethoxyflavone (HMF) to prevent obesity and regulate lipid metabolism in vivo. We aimed to investigate the potential efficacy of HMF on preventing obesity and hyperlipidemia in rats fed a high-fat diet (HFD) and its underlying mechanisms. Male Sprague–Dawley rats were fed a normal diet or an HFD with or without HMF (0.02%, 0.04% and 0.08%, w/w) for 6 weeks. The supplementation of HMF not only significantly decreased body weight gain (HFD, 336.50 ± 18.84 g; LHMF, 309.43 ± 20.74 g; MHMF, 296.83 ± 13.88 g; HHMF, 265.71 ± 19.09 g; respectively, p < 0.05) and adipose tissues weight (p < 0.05), but also markedly lowered serum levels of total cholesterol, triacylglycerol, and low-density lipoprotein cholesterol (p < 0.05) in the sixth week in a dose-dependent manner compared with the HFD group. HMF also significantly alleviated hepatic steatosis in the liver (liver weight g/100 g body weight of HFD, 4.86 ± 0.11%; LHMF, 4.02 ± 0.33%; MHMF, 4.05 ± 0.31%; HHMF, 3.72 ± 0.34%; respectively, p < 0.05). Furthermore, transcriptome analysis and real-time quantitative RT-PCR demonstrated that HMF supplementation markedly downregulated hepatic genes related to adipogenesis transcription and inflammatory responses, and significantly upregulated genes related to fatty acid oxidation and energy expenditure. These results indicated that HMF could effectively prevent obesity and hyperlipidemia by regulation of the expression of lipid metabolism-related and inflammatory response-related genes.