The potential role of beef and nutrients found in beef on outcomes of wellbeing in healthy adults 50 years of age and older: A systematic review of randomized controlled trials.

Shifts in wellbeing and health occur as we age. As life expectancy increases, maintenance of wellbeing and health becomes increasingly important. Nutrients found in beef are associated with outcomes of wellbeing such as physical and cognitive function, lean body mass, and mood in older adults and individuals with chronic disease. However, it is unclear how beef and nutrients found in beef impact wellbeing in healthy adults ≥50 years of age. This study systematically reviewed evidence linking the intake of beef and nutrients found in beef to markers of wellbeing in healthy adults. PubMed, CINAHL, and Web of Science were searched up to August 31, 2021 for eligible randomized controlled trials (RCTs). Nutrients included in the analysis were beef, red meat, dietary protein, essential amino acids, branched chain amino acids, tryptophan, arginine, cysteine, glycine, glutamate, vitamin B6, vitamin B12, choline, zinc, and iron. We identified nine RCTs with results from 55 measurements of markers of wellbeing. An overall positive effect was found of beef and beef's nutrients on wellbeing. There was an overall positive effect of amino acids and protein on wellbeing, with no effect of arginine, vitamin B-12, leucine, and zinc. Physical function was also influenced by beef and nutrients found in beef. Eight of the studies found focused on specific nutrients found in beef, and not beef itself in older adults with one or more chronic diseases. This study identified a need for further research regarding the effect of beef and nutrients found in beef on defined functional outcomes of wellbeing in healthy adults ≥50 years of age.

Net protein balance correlates with expression of autophagy, mitochondrial biogenesis, and fat metabolism-related genes in skeletal muscle from older adults.

The mechanisms leading to sarcopenia, the main cause for frailty in older adults, are still unclear. Autophagy and the ubiquitin-proteasome system (UPS) may play a role in mediating muscle protein breakdown related to sarcopenia. In addition to loss of muscle mass, compromised muscle performance observed in sarcopenic patients has been linked to muscle mitochondria dysfunction. Increased fat deposition and fat cell infiltration in muscle frequently seen in skeletal muscle of older adults may play an additional role for the pathogenesis of sarcopenia. Therefore, the first objective of this study was to understand differences in expression of genes related to autophagy, UPS, mitochondrial biogenesis, and fat metabolism in skeletal muscle of older adults compared with young adults. Our second objective was to determine the correlation between whole body protein kinetics (WBPK) and gene expression with age. Real-time quantitative PCR was used to determine the relative expression of targeted genes, and hierarchical regression analysis was used to determine if age had a moderating effect on the correlation between expression of targeted genes and WBPK. Increases in the expression of autophagy-related genes and fat metabolism-related genes were observed in muscle of older adults compared with young adults. In addition, age enhanced the negative correlations between mitochondrial biogenesis genes and net protein balance. These results suggest that dysregulated gene expression of mitochondrial biogenesis could play a role in muscle loss in older adults.

Leucine decreases intramyocellular lipid deposition in an mTORC1-independent manner in palmitate-treated C2C12 myotubes.

Higher intramyocellular lipid (IMCL) deposition in skeletal muscle is commonly observed in patients with obesity, resulting in mitochondrial damage. Palmitic acid, a saturated fatty acid, has been reported to induce obesogenic conditions in C2C12 myotubes. Leucine has been shown to improve obesity-related metabolic signatures; however, evidence for the effect of leucine on IMCL and the underlying mechanisms are still lacking. The objective of this study was to determine the effect of leucine on IMCL deposition and identify the potential mechanisms. Palmitate-treated C2C12 myotubes were used as an in vitro model of obesity. Two doses of leucine were used: 0.5 mM (postprandial physiological plasma concentration) and 1.5 mM (supraphysiological plasma concentration). Rapamycin was used to determine the role of mammalian target of rapamycin complex 1 (mTORC1) in leucine's regulation of lipid deposition in C2C12 myotubes. One-way ANOVA followed by Tukey's post hoc test was used to calculate differences between treatment groups. Our results demonstrate that leucine reduces IMCL deposition in an mTORC1-independent fashion. Furthermore, leucine acts independently of mTORC1 to upregulate gene expression related to fatty acid metabolism and works through both mTORC1-dependent and mTORC1-independent pathways to regulate mitochondrial biogenesis in palmitate-treated C2C12 myotubes. In agreement with increased mitochondrial biogenesis, increased mitochondrial content, circularity, and decreased autophagy are observed in the presence of 1.5 mM leucine. Taken together, the results indicate leucine reduces IMCL potentially through an mTORC1-independent pathway in palmitate-treated C2C12 myotubes.

A High-Protein Diet Reduces Weight Gain, Decreases Food Intake, Decreases Liver Fat Deposition, and Improves Markers of Muscle Metabolism in Obese Zucker Rats.

A primary factor in controlling and preventing obesity is through dietary manipulation. Diets higher in protein have been shown to improve body composition and metabolic health during weight loss. The objective of this study was to examine the effects of a high-protein diet versus a moderate-protein diet on muscle, liver and fat metabolism and glucose regulation using the obese Zucker rat. Twelve-week old, male, Zucker (fa/fa) and lean control (Fa/fa) rats were randomly assigned to either a high-protein (40% energy) or moderate-protein (20% energy) diet for 12 weeks, with a total of four groups: lean 20% protein (L20; n = 8), lean 40% protein (L40; n = 10), obese 20% protein (O20; n = 8), and obese 40% protein (O40; n = 10). At the end of 12 weeks, animals were fasted and euthanized. There was no difference in food intake between L20 and L40. O40 rats gained less weight and had lower food intake (p < 0.05) compared to O20. O40 rats had lower liver weight (p < 0.05) compared to O20. However, O40 rats had higher orexin (p < 0.05) levels compared to L20, L40 and O20. Rats in the L40 and O40 groups had less liver and muscle lipid deposition compared to L20 and L40 diet rats, respectively. O40 had decreased skeletal muscle mechanistic target of rapamycin complex 1 (mTORC1) phosphorylation and peroxisome proliferator-activated receptor gamma (PPARγ) mRNA expression compared to O20 (p < 0.05), with no difference in 5' AMP-activated protein kinase (AMPK), eukaryotic translation initiation factor 4E binding protein 1 (4EBP1), protein kinase B (Akt) or p70 ribosomal S6 kinase (p70S6K) phosphorylation. The data suggest that high-protein diets have the potential to reduce weight gain and alter metabolism, possibly through regulation of an mTORC1-dependent pathway in skeletal muscle.