Duyun compound green tea (DCGT) is a healthy beverage with lipid-lowering effect commonly consumed by local people, but its mechanism is not very clear. We evaluated the effect of DCGT treatment on bile acids (BA) metabolism of mice with high-fat diet (HFD) – induced hyperlipidaemia by biochemical indexes and metabolomics and preliminarily determined the potential biomarkers and metabolic pathways of hyperlipidaemia mice treated with DCGT as well as investigated its lipid-lowering mechanism. The results showed that DCGT treatment could reduce HFD – induced gain in weight and improve dyslipidaemia. In addition, a total of ten types of BA were detected, of which seven changed BA metabolites were observed in HFD group mice. After DCGT treatment, glycocholic acid, tauroursodeoxycholic acid and taurochenodeoxycholic acid were significantly down-regulated, while hyodeoxycholic acid, deoxycholic acid and chenodeoxycholic acid were markedly up-regulated. These results demonstrated that DCGT treatment was able to make the BA metabolites in the liver of hyperlipidaemia mice normal and alleviate hyperlipidaemia by regulating the metabolites such as glycocholic acid, tauroursodeoxycholic acid and taurochenodeoxycholic, as well as the BA metabolic pathway and cholesterol metabolic pathway involved.

Overweight-related metabolic diseases are an important threat to health in the Western world. Dietary habits are one of the main causative factors for metabolic syndrome, CVD and type 2 diabetes. The human gut microbiota is emerging as an important player in the interaction between diet and metabolic health. Gut microbial communities contribute to human metabolism through fermentation of dietary fibre and the result of intestinal saccharolytic fermentation is production of SCFA. Acetate, propionate and butyrate positively influence satiety, endocrine system, glucose homeostasis, adipogenesis, lipid oxidation, thermoregulation, hepatic gluconeogenesis, endothelial function and gut barrier integrity, and these mechanisms have all been linked to protection from type 2 diabetes, hypertension and cardiovascular health. The gut microbiota is also involved in bile acid metabolism and regulating their cell signalling potential, which has also been shown to modify pathways involved in metabolic health. Similarly, the gut microbiota renders recalcitrant plant polyphenols into biologically active small phenolic compounds which then act systemically to reduce metabolic disease risk. This review summarises how dietary patterns, specific foods and a healthy lifestyle may modulate metabolic health through the gut microbiota and their molecular cross-talk with the host.

Legalized trade in commercially farmed wildlife products is sometimes promoted as a conservation strategy. In theory, flooding the market with cheaper or better quality products will decrease the profitability of poaching. Bear bile is highly sought-after for use in traditional medicine and overhunting to supply the demand for bear parts has led to declining populations across South-east Asia. Bear bile farming was established to help supply the high demand for bear bile. In Viet Nam it is legal to keep registered bears, but illegal to extract or sell bear bile. We conducted semi-structured interviews with 66 bear bile farmers in Viet Nam to examine the conservation implications of bear bile farming. The results show that demand for wild bear bile was not satisfied by the widespread availability of farmed bear bile. Farmers report a strong consumer preference and willingness to pay more for wild-sourced products. The existence of bear bile farms presents considerable challenges to law enforcement. The results suggest that bear bile farming in Viet Nam relies on restocking from wild populations, and farmers openly admit to extracting and selling bear bile, in clear violation of national legislation. The case of bear bile farming in Viet Nam provides an example of wildlife farming failing to reduce pressure on a once widely distributed and relatively abundant species. Research into consumer values, attitudes and behaviours will help to improve understanding of market drivers and help inform the design of effective species conservation and management strategies.

The intestine is the only gate for the entry of Ca to the body in humans and mammals. The entrance of Ca occurs via paracellular and intracellular pathways. All steps of the latter pathway are regulated by calcitriol and by other hormones. Dietary and pharmacological compounds also modulate the intestinal Ca absorption process. Among them, dietary Ca and P are known to alter the lipid and protein composition of the brush-border and basolateral membranes and, consequently, Ca transport. Ca intakes are below the requirements recommended by health professionals in most countries, triggering important health problems. Chronic low Ca intake has been related to illness conditions such as osteoporosis, hypertension, renal lithiasis and incidences of human cancer. Carbohydrates, mainly lactose, and prebiotics have been described as positive modulators of intestinal Ca absorption. Apparently, high meat proteins increase intestinal Ca absorption while the effect of dietary lipids remains unclear. Pharmacological compounds such as menadione, dl-butionine-S,R-sulfoximine and ursodeoxycholic acid also modify intestinal Ca absorption as a consequence of altering the redox state of the epithelial cells. The paracellular pathway of intestinal Ca absorption is poorly known and is under present study in some laboratories. Another field that needs to be explored more intensively is the influence of the gene × diet interaction on intestinal Ca absorption. Health professionals should be aware of this knowledge in order to develop nutritional or medical strategies to stimulate the efficiency of intestinal Ca absorption and to prevent diseases.

The consumption of lipids and simple sugars induces an inflammatory response whose exact molecular trigger remains elusive. The aims of the present study were to investigate (1) whether inflammation induced by a single high-energy, high-fat meal (HFM) is associated with endoplasmic reticulum stress (ERS) in peripheral blood mononuclear cells (PBMC) and (2) whether these inflammatory and ERS responses could be prevented by the chemical chaperone ursodeoxycholic acid (UDCA). A total of ten healthy lean men were recruited to a randomised, blind, cross-over trial. Subjects were given two doses of placebo (lactose) or UDCA before the consumption of a HFM (6151 kJ; 47·4 % lipids). Blood was collected at baseline and 4 h after the HFM challenge. Cell populations and their activation were analysed using flow cytometry, and plasma levels of inflammatory cytokines were assessed by ELISA and Luminex technology. Gene expression levels of inflammatory and ERS markers were analysed in CD14+ and CD14− PBMC using quantitative RT-PCR. The HFM induced an increase in the mRNA expression levels of pro-inflammatory cytokines (IL-1β, 2·1-fold; IL-8, 2·4-fold; TNF-α, 1·4-fold; monocyte chemoattractant protein 1, 2·1-fold) and a decrease in the expression levels of miR181 (0·8-fold) in CD14+ monocytes. The HFM challenge did not up-regulate the expression of ERS markers (XBP1, HSPA5, EDEM1, DNAJC3 and ATF4) in either CD14+ or CD14− cell populations, except for ATF3 (2·3-fold). The administration of UDCA before the consumption of the HFM did not alter the HFM-induced change in the expression levels of ERS or inflammatory markers. In conclusion, HFM-induced inflammation detectable on the level of gene expression in PBMC was not associated with the concomitant increase in the expression levels of ERS markers and could not be prevented by UDCA.

We investigated the feasibility of increasing ursodeoxycholic acid (UDCA) in the enterohepatic circulation of pigs by administering living bacteria capable of epimerising endogenous amidated chenodeoxycholic acid (CDCA) to UDCA. We first demonstrated that combining Bifidobacterium animalis DN-173 010, as a bile salt-hydrolysing bacterium, and Clostridium absonum ATCC 27555, as a CDCA to UDCA epimerising bacterium, led to the efficient epimerisation of glyco- and tauro-CDCA in vitro, with respective UDCA yields of 55·8 (se 2·8) and 36·6 (se 1·5)%. This strain combination was then administered to hypercholesterolaemic pigs over a 3-week period, as two daily preprandial doses of either viable (six experimental pigs) or heat-inactivated bacteria (six controls). The main effects of treatment were on unconjugated bile acids (P=0·035) and UDCA (P<0·0001) absorbed into the portal vein, which increased 1·6–1·7- and 3·5–7·5-fold, respectively, under administration of living compared with inactivated bacteria. In bile, UDCA did not increase significantly, but the increase in biliary lithocholic acid with time in the controls was not observed in the experimental pigs (P=0·007), and the same trend was observed in faeces. All other variables (biliary lipid equilibrium, plasma lipid levels and partition of cholesterol between the different lipoprotein classes) remained unaffected by treatment throughout the duration of the experiment. In conclusion, it is feasible to increase the bioavailability of UDCA to the intestine and the liver by administering active bacteria. This may represent an interesting new probiotic activity, provided that in future it could be expressed by a safe food micro-organism.