The impact of dietary soybean oil, lard and fish oil on physiological responses in middle age is little studied. In this study, we investigated the changes of oxidative stress, inflammatory cytokines, telomere length, and age-related gene expression in the liver of middle-aged rats in response to the above three fat diets. Male Sprague Dawley rats (12 months old) were fed AIN-93M diets for 3 months, in which soybean oil was equivalently replaced by lard or fish oil. As compared to the lard diet, intake of fish oil diet significantly decreased body weight gain, white blood cell count, and levels of hepatic triacylglycerol, total cholesterol, fat accumulation, low-density lipoprotein, oxidative stress and inflammatory cytokines (P < 0.05), but increased telomere length (P < 0.05). On the other hand, lard diet and soybean oil diet showed great similarity in the above variables. PCR array analysis further indicated that fish oil diet significantly down-regulated gene expression related to inflammatory response, apoptosis, DNA binding, proteostasis and telomere attrition. Differentially expressed genes were enriched in the complement and coagulation cascades pathways. Such physiological and molecular responses could be due to different fatty acid composition in fish oil, lard and soybean oil.

ScopeDietary fats have been shown to affect gut microbiota composition and aging gene expression of middle‐aged rats at a normal dose, but little is known about such an effect on gut barrier. In this study, the changes in colonic Muc2 expression are investigated and the underlying mechanism is also proposed.Methods and results36 middle‐aged Sprague–Dawley rats are assigned to one of the diets containing soybean oil, lard, or fish oil (4%). The rats are fed for 5 weeks and then goblet cells, Muc2 expression, and inflammatory cytokines in the colon are measured. Proteome analysis is performed. Compared with the lard and soybean oil diet groups, intake of fish oil decreases the number of goblet cells, and inhibits Muc2 and TLRs expression in the colon of middle‐aged rats, which would impair mucus barrier. Several key enzymes involved in glycosylation process, including Agr2, Gale, Gne, Pmm2, Pdxdc1, Plch1, Pfkp, Cmpk1, and Rexo2, show the lowest abundance in the fish oil diet group.ConclusionIntake of fish oil at a normal dose downregulates colonic Muc2 expression. This negative effect of fish oil may involve the suppression of mucin glycosylation process.

In this work, the effects of different sources of meat protein on liver metabolic enzymes were investigated. Rats were fed for 90 days with semisynthetic diets in which casein was fully replaced by isolated soybean, fish, chicken, pork, or beef proteins. Then, liver proteomics was performed using iTRAQ and LC-ESI-MS/MS. The results indicated that intake of meat protein diets significantly reduced the protein levels of CYP450s, GSTs, UGTs, and SULTs compared to those of the casein and soybean protein diet groups. The total antioxidant capacity and lipid peroxidation values did not differ between four meat protein diet groups and the casein diet group. However, GSH activity in the fish, chicken, and beef protein groups was significantly higher than those of the casein and soybean protein groups. The beef protein diet significantly upregulated the expression of immune-related proteins. The Keap1-Nrf2-ARE signaling pathway was suggested to involve the diet-mediated regulation of biotransformation, inflammation, and redox status.

Meat consumption is gradually increasing and its impact on health has attracted widespread attention, resulting in epidemiological studies proposing a reduction in meat and processed meat intake. This review briefly summarizes recent advances in understanding the effects of meat or processed meat on human health, as well as the underlying mechanisms. Meat consumption varies widely among individuals, populations, and regions, with higher consumption in developed countries than in developing countries. However, increasing meat consumption may not be the main cause of increasing incidence of chronic disease, since the development of chronic disease is a complex physiological process that involves many factors, including excessive total energy intake and changes in food digestion processes, gut microbiota composition, and liver metabolism. In comparison, unhealthy dietary habits and a sedentary lifestyle with decreasing energy expenditure are factors more worthy of reflection. Meat and meat products provide high‐value protein and many key essential micronutrients. In short, as long as excessive intake and overprocessing of meats are avoided, meat remains an indispensable source of nutrition for human health.

Casein and chicken are assessed to contain high quality proteins, which are essential for human health. Studies have shown that ingestion of the two dietary proteins resulted in distinct effects on physiology, liver transcriptome and gut microbiota. However, its underlying mechanism is not fully understood, in particular for a crosstalk between gut microbiota and host under a specific diet intervention. We fed young rats with a casein or a chicken protein-based diet (CHPD) for 7 days, and characterized cecal microbiota composition and cecal gene expression. We found that a short-term intervention with a casein-based diet (CAD) induced a higher relative abundance of beneficial bacterium Lactococcus lactis as well as Bifidobacterium pseudolongum, which upregulated galactose metabolism of the microbiome compared with a CHPD. The CAD also upregulated gene expression involved in obesity associated pathways (e.g., Adipoq and Irs1) in cecal tissue of rats. These genes and the bacterial taxon were reported to play an important role in protecting development of obesity. Furthermore, the differentially represented bacterial taxon L. lactis was positively associated with these differentially expressed genes in the gut tissue. Our results provide a new insight into the crosstalk between gut microbiota and host in response to dietary proteins, indicating a potential mechanism of obesity prevention function by casein.