Oxidative stress is a status of imbalance between oxidants and antioxidants, resulting in molecular damage and interruption of redox signaling in an organism. Indeed, oxidative stress has been associated with many metabolic disorders due to unhealthy dietary patterns and may be alleviated by properly increasing the intake of antioxidants. Thus, it is quite important to adopt a healthy dietary mode to regulate oxidative stress and maintain cell and tissue homeostasis, preventing inflammation and chronic metabolic diseases. This review focuses on the links between dietary nutrients and health, summarizing the role of oxidative stress in ‘unhealthy’ metabolic pathway activities in individuals and how oxidative stress is further regulated by balanced diets.

Isolating and maintaining the appropriate stem cell for large scale cell culture is essential in tissue engineering or food production. For bovine satellite cells an optimized isolation and purification protocol is lacking and there is also no detailed understanding on the factors that maintain stemness of these cells. Here, we set up a fluorescence-activated cell sorting strategy to enrich bovine satellite cells. We found that p38-MAPK signalling is activated and PAX7 expression is gradually lost during satellite cell proliferation. The p38 inhibitor (SB203580) treatment maintained PAX7 expression but inhibited the fusion of satellite cells in a concentration-dependent way in short-term incubation. The mechanism of p38 inhibition was confirmed by inhibiting canonical p38 signalling, i.e. HSP27. Long-term culture with an appropriate concentration of p38i enhanced the proliferation and PAX7 expression, while the differentiation capacity recovered and was enhanced compared to vehicle control. These studies indicate that bovine satellite cells maintenance depends on cell purity and p38 MAPK signalling. Inhibition of p38 MAPK signaling is a promising strategy to facilitate large scale cell expansion of primary cells for tissue engineering and cultured meat purposes.

Consumption of dietary protein at recommended levels is considered a potential strategy to promote satiety and weight management, but how protein from different dietary sources effect the obesity development, lipid metabolism, and gut microbiota is not known. This study focused on the effects of beef, casein, and soy protein diet on lipid metabolism, triglycerides accumulation, and microbial diversity in colon of C57BL/6J mice, which were given either low-fat diets (LFD, 12% Kcal) or high-fat diets (HFD, 60% Kcal) for 12 weeks. Body and liver weight increased significantly in mice fed a beef protein HFD (HFB), whereas reduced cumulative energy intake was seen in a soy protein HFD (HFS) group. HFB-fed mice showed signs of impaired glucose metabolism and insulin resistance along with a significant elevation in the concentration of triglycerides, LDL-cholesterol, total cholesterol, IL1β, TNF-α, IL-6, and leptin in serum. HFB also enhanced lipid accumulation in liver with increased activity of genes important for lipogenesis and hepatic cholesterol metabolism. A 16S rRNA gene sequencing indicated that HFD, regardless of proteins, significantly enhanced the ratio of Firmicutes to Bacteroidetes in colonic microbiota. However, HFB not only reduced the abundance of Akkermansia, compared with LFD independent of proteins, but also decreased the abundance of butyrate-producing bacteria such as Anaerotruncus, Butyricicoccus, and Lactobacillus (P < 0.05) compared with HFS and HFC. In conclusion, consumption of HFB does not only affect the gut microbiota composition but also increases the problems related to metabolic syndromes like dyslipidemia, hypercholesterolemia, and triglycerides accumulation in liver, which lead to systemic inflammation and its associated comorbidities, for example, impaired glucose metabolism and insulin resistance.

High-salt diet has been considered to cause health problems, but it is still less known how high-salt diet affects gut microbiota, protein digestion, and passage in the digestive tract. In this study, C57BL/6J mice were fed low- or high-salt diets (0.25 vs. 3.15% NaCl) for 8 weeks, and then gut contents and feces were collected. Fecal microbiota was identified by sequencing the V4 region of 16S ribosomal RNA gene. Proteins and digested products of duodenal, jejunal, cecal, and colonic contents were identified by LC-MS-MS. The results indicated that the high-salt diet increased Firmicutes/Bacteroidetes ratio, the abundances of genera Lachnospiraceae and Ruminococcus (P < 0.05), but decreased the abundance of Lactobacillus (P < 0.05). LC-MS-MS revealed a dynamic change of proteins from the diet, host, and gut microbiota alongside the digestive tract. For dietary proteins, high-salt diet seemed not influence its protein digestion and absorption. For host proteins, 20 proteins of lower abundance were identified in the high-salt diet group in duodenal contents, which were involved in digestive enzymes and pancreatic secretion. However, no significant differentially expressed proteins were detected in jejunal, cecal, and colonic contents. For bacterial proteins, proteins secreted by gut microbiota were involved in energy metabolism, sodium transport, and protein folding. Five proteins (cytidylate kinase, trigger factor, 6-phosphogluconate dehydrogenase, transporter, and undecaprenyl-diphosphatase) had a higher abundance in the high-salt diet group than those in the low-salt group, while two proteins (acetylglutamate kinase and PBSX phage manganese-containing catalase) were over-expressed in the low-salt diet group than in the high-salt group. Consequently, high-salt diet may alter the composition of gut microbiota and has a certain impact on protein digestion.