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Aim: Meat and its derivatives provide nutrients essential for human health. However, meat consumption, along with excessive fat intake, has been associated with gut inflammation, intestinal barrier dysfunction and alterations in gut microbiota. Herein, we investigated whether and how these changes in the intestinal barrier system affect the gut liver axis and hepatic injury and eventually lead to the progression of liver syndrome such as NAFLD., Methods: Mice were fed with high fat (60% kcal) or low fat (12% kcal) along with soybean (control), chicken and pork proteins (HFCH, HFP, LFCH, and LFP) for 12 weeks. The biomarkers for liver injury were investigated after meat protein intake along with the high fat., Findings: Greater amount of fat vacuoles visible in the H&E staining increased the inflammatory cell infiltration and disorganized liver structures were observed in the HFP-fed mice. Oil Red O staining revealed that the HFP-fed and HFCH-fed mice showed more lipid droplets, confirming the increased hepatic lipid accumulation. Potential serum markers for NAFLD, ALT and AST were increased in the HF meat diet groups. Key genes responsible for hepatic inflammation and lipogenesis, such as MCP-1, IL1-β and TNF-α were upregulated. HF meat protein diet-fed mice exhibited signs of compromised liver with increased levels of endotoxin in the liver and its binding protein in serum, upregulation of TLRs in the liver, and significant increase in TG, TC, LDL-C and HDL-C concentrations., Significance: Intestinal inflammation and barrier dysfunction aggravate liver injury and fibrosis due to the intake of HF meat protein diets in mice, which may contribute to the progress of liver injury and associated complications. Gut inflammation may directly contribute to the development of NAFLD, especially of the gut vascular barricade dysfunction.

Endocannabinoids modulate insulin and adipokine expression in adipocytes through cannabinoid receptors and their levels are elevated during hyperglycemia and obesity, but little is known about how diets affect them. We assessed the effects of dietary casein, chicken, beef, and pork proteins in a high-fat diet mode, on endocannabinoids, adipogenesis, and biomarkers associated with dyslipemdia. A high-fat beef or chicken diet upregulated cannabinoid 1 receptor, N -acyl phosphatidylethanolamine-selective phospholipase-D and diacylglycerol lipase α in adipose tissue and reduced the immunoreactivity of mitochondrial uncoupling protein 1 in brown adipose tissue. In addition, the high-fat diets with beef and chicken protein had a significant impact on adipocyte differentiation and mitochondrial biogenesis in obese mice. A 16S rRNA gene sequencing indicated that high-fat diets, regardless of the protein source, significantly enhanced the ratio of Firmicutes to Bacteroidetes in colon. Meat proteins in a high-fat diet significantly decreased the relative abundances of Akkermansia and Bifidobacteria but enhanced the lipopolysaccharides level in the serum, which promoted the adipogenesis process by causing dysregulation in the endocannabinoid receptors. Consumption of meat protein with high-fat-induced adiposity, visceral obesity, and dyslipidemia reduced the thermogenesis and had a distinctive effect on the mitochondrial biogenesis compared with casein protein.

Protein supplementation might improve body composition and exercise performance. Supplements containing whey protein (WP) have received the most attention, but other protein sources such as beef protein (BP) are gaining popularity. We conducted a systematic review and meta-analysis of randomized controlled trials that compared the effects of exercise training combined with BP, WP or no protein supplementation (NP), on body composition or exercise performance. Secondary endpoints included intervention effects on total protein intake and hematological parameters. Seven studies ( n = 270 participants) were included. No differences were found between BP and WP for total protein intake (standardized mean difference (SMD) = 0.04, p = 0.892), lean body mass (LBM) (SMD = -0.01, p = 0.970) or fat mass (SMD = 0.07, p = 0.760). BP significantly increased total daily protein intake (SMD = 0.68, p < 0.001), LBM (SMD = 0.34, p = 0.049) and lower-limb muscle strength (SMD = 0.40, p = 0.014) compared to NP, but no significant differences were found between both conditions for fat mass (SMD = 0.15, p = 0.256), upper-limb muscle strength (SMD = 0.16, p = 0.536) or total iron intake (SMD = 0.29, p = 0.089). In summary, BP provides similar effects to WP on protein intake and body composition and, compared to NP, might be an effective intervention to increase total daily protein intake, LBM and lower-limb muscle strength.

Background and objectives: The anemia is the most common extra-intestinal manifestation of the ulcerative colitis. Taking into account, that meat products are perceived as factor, that may promote relapses, the crucial is to indicate the dietary recommendations to prevent anemia development but without high animal products intake. Aim of the study was to analyze the influence of animal products intake on the red blood cell count results in remission ulcerative colitis individuals and pair-matched control group, during 6 weeks of observation. Materials and Methods: The intake of nutrients associated with anemia development (iron, vitamin B 12 , protein, animal protein, calcium) and the products being their sources (meat, meat products, dairy beverages, cottage cheese, rennet cheese) were analyzed. Results: In spite of the higher meat products intake in the group of ulcerative colitis individuals, the iron intake did not differ between groups. The positive correlations between intakes of meat, meat products, total protein, animal protein, iron, vitamin B 12 and red blood cell count results were stated for ulcerative colitis individuals, while in control group were not observed, that may have resulted from higher susceptibility for the diet-influenced changes. Conclusions: The positive correlation between red blood cell count results and energy value of diet, and daily iron intake observed in ulcerative colitis individuals, accompanied by negative correlation for iron intake per 1000 kcal of diet, may indicate, that higher iron intake may be beneficial, but only while accompanied by high energy value of diet., Competing Interests: The authors declare no conflict of interest.

Inflammatory bowel disease (IBD), a collective term for Crohn disease and ulcerative colitis, is a polygenic disease thought to be triggered by environmental factors. A Western or westernized lifestyle may be a major driver of the growing incidence of IBD. IBD may represent dysregulated mucosal inflammation to gut microbiota. Despite many review articles on environmental factors in IBD, no consensus exists regarding which factor contributes most to trigger the onset of IBD. Identification and recognition of major environmental factors are prerequisite for effective disease treatment and prevention. Representative environmental factors such as smoking, breastfeeding, nonsteroidal anti-inflammatory drugs, antibiotic use in childhood, oral contraceptives, and appendectomy do not correlate with disease onset in most patients with IBD. In contrast, diet appears to be important in most cases of IBD. Diets rich in animal protein (risk factor) and deficient in dietary fiber (preventive factor) are characteristic of westernized diets in affluent societies. Recent research shows that westernized diets are associated with a reduced gut microbial diversity (dysbiosis), which may result in increased susceptibility to IBD and other common chronic diseases. Plant-based diets rich in dietary fiber are associated with increased microbial diversity. Recent reports on IBD therapy that replaced westernized diets with plant-based diets achieved far better outcomes than those previously reported in the literature. We believe that westernized diet-associated gut dysbiosis is the most ubiquitous environmental factor in IBD. Adoption of this concept may have the potential to provide a better quality of life for patients with IBD.