Possible Extracellular Signals to Ameliorate Sarcopenia in Response to Medium-Chain Triglycerides (8:0 and 10:0) in Frail Older Adults.

In frail older adults (mean age 85 years old), a 3-month supplementation with a low dose (6 g/day) of medium-chain triglycerides (MCTs; C8:0 and C10:0) given at a meal increased muscle mass and function, relative to supplementation with long-chain triglycerides (LCTs), but it decreased fat mass. The reduction in fat mass was partly due to increased postprandial energy expenditure by stimulation of the sympathetic nervous system (SNS). However, the extracellular signals to ameliorate sarcopenia are unclear. The following three potential extracellular signals to increase muscle mass and function after MCT supplementation are discussed: (1) Activating SNS-the hypothesis for this is based on evidence that a beta2-adrenergic receptor agonist acutely (1-24 h) markedly upregulates isoforms of peroxisomal proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha) mRNAs, promotes mitochondrial biogenesis, and chronically (~1 month) induces muscle hypertrophy. (2) An increased concentration of plasma acyl-ghrelin stimulates growth hormone secretion. (3) A nitrogen-sparing effect of ketone bodies, which fuel skeletal muscle, may promote muscle protein synthesis and prevent muscle protein breakdown. This review will help guide clinical trials of using MCTs to treat primary (age-related) sarcopenia.

The thermal dependence of the protein-sparing effect in rainbow trout (Oncorhynchus mykiss, Walbaum 1792).

The authors performed an instantaneous bioenergetic study with rainbow trout (Oncorhynchus mykiss) of 206.3 g ± 2.9 g in a group respirometer of nine 250 l tanks at five different water temperatures (12, 14, 16, 18, 20°C) to determine the optimal thermal condition for a maximal visualization of the protein-sparing effect. Twelve fish per tank were tested at a stocking density of 9.94 kg m-3 ± 0.14 kg m-3 and fed three low-protein/high-energy diets with constant crude protein content of c. 35% and three different energy contents (17.35, 18.76, 20.50 MJ kg-1 ) once daily at a ration of 1.3% body weight (n = 3). Energy levels were increased by adding gelatinized wheat starch as a carbohydrate source and fish oil, canola oil and palmitin as lipid sources. Three different dietary digestible protein/digestible energy ratios (DP/DE: 20.38, 19.08, 18.09 mg kJ-1 ) were achieved by replacing bentonite as a non-nutritive filler with carbohydrates and lipids. Oxygen consumption and ammonia excretion were assessed to obtain the potentially retainable energy (RE) and ammonia quotient (AQ) as benchmarks for potential growth and protein-sparing effect. The results showed the lowest relative metabolic combustion of protein at 16.9°C ± 0.1°C. The authors determined this temperature to set the optimal thermal condition for the induction of a maximum protein-sparing effect in juvenile rainbow trout. Increasing the DP/DE ratio significantly altered the magnitude of the relative metabolic protein use but had no effect on its interactions with temperature. The authors were able to reduce average metabolic fuel use of protein across diets from 16.2% ± 2.3% at 12°C to 8.0% ± 1.2% at 16°C. This study found no relevant significant differences of RE with the environmental temperature.

Interactive effects of protein and energy intake on nutrient partitioning and growth in Nile tilapia.

Studies of fish growth response to changes in dietary protein and energy content are often conducted with fish fed to apparent satiation or at fixed percentages of their body mass. Such designs result in simultaneous changes in protein and non-protein energy intake, thereby failing to distinguish their separate effects on nutrient partitioning and growth. The present study was designed to address this limitation and test the existence of distinct protein- and non-protein energy-dependent growth phases in Nile tilapia (Oreochromis niloticus). All-male Nile tilapia (63 g, SD = 1.3) were subjected to an 8 × 2 factorial design consisting of eight levels of digestible protein (DP) intake (0.44-1.25 g/day) and two levels of non-protein digestible energy (NPDE) intake (16.0 and 22.4 kJ/day). Fish (n = 960) were housed in 60-litre tanks with two replicates per treatment and hand-fed twice a day for 42 days. Nutrient balances were calculated from changes in body mass, analysed body composition and digestible nutrient intake. Linear regression models were compared to linear-plateau regression models to determine whether protein gain followed distinct protein- and non-protein energy-dependent phases or not. Body mass gain increased linearly with increasing DP intake and was significantly higher (2.6 vs 2.3 g/d, P < 0.05) in fish receiving a high NPDE intake. This increase mainly reflected a higher mean fat gain (0.29 vs 0.20 g/d) rather than a higher protein gain (0.42 vs 0.39 g/d) in fish fed a high vs low level of NPDE intake. The comparison of linear and linear-plateau models did not give clear support for the presence of distinct protein and non-protein energy-dependent phases in protein gain. These results indicate that non-protein energy intake has a modest protein-sparing potential, and that protein gain is simultaneously limited by protein and energy intake in Nile tilapia.

The protein-sparing effect of α-lipoic acid in juvenile grass carp, Ctenopharyngodon idellus: effects on lipolysis, fatty acid ß-oxidation and protein synthesis.

To investigate the protein-sparing effect of α-lipoic acid (LA), experimental fish (initial body weight: 18·99 (sd 1·82) g) were fed on a 0, 600 or 1200 mg/kg α-LA diet for 56 d, and hepatocytes were treated with 20 µm compound C, the inhibitor of AMP kinase α (AMPKα), treated for 30 min before α-LA treatment for 24 h. LA significantly decreased lipid content of the whole body and other tissues (P0·05). Consistent with results from the experiment in vitro, LA activated phosphorylation of AMPKα and notably increased the protein content of adipose TAG lipase in intraperitoneal fat, hepatopancreas and muscle in vivo (P<0·05). Meanwhile, LA significantly up-regulated the mRNA expression of genes involved in fatty acid ß-oxidation in the same three areas, and LA also obviously down-regulated the mRNA expression of genes involved in amino acid catabolism in muscle (P<0·05). Besides, it was observed that LA significantly activated the mammalian target of rapamycin (mTOR) pathway in muscle of experimental fish (P<0·05). LA could promote lipolysis and fatty acid ß-oxidation via increasing energy supply from lipid catabolism, and then, it could economise on the protein from energy production to increase protein deposition in grass carp. Besides, LA might directly promote protein synthesis through activating the mTOR pathway.

How Much and What Type of Protein Should a Critically Ill Patient Receive?

Protein loss, manifested as loss of muscle mass, is observed universally in all critically ill patients. Depletion of muscle mass is associated with impaired function and poor outcomes. In extreme cases, protein malnutrition is manifested by respiratory failure, lack of wound healing, and immune dysfunction. Protecting muscle loss focused initially on meeting energy requirements. The assumption was that protein was being used (through oxidation) as an energy source. In healthy individuals, small amounts of glucose (approximately 400 calories) protect muscle loss and decrease amino acid oxidation (protein-sparing effect of glucose). Despite expectations of the benefits, the high provision of energy (above basal energy requirements) through the delivery of nonprotein calories has failed to demonstrate a clear benefit at curtailing protein loss. The protein-sparing effect of glucose is not clearly observed during illness. Increasing protein delivery beyond the normal nutrition requirements (0.8 g/k/d) has been investigated as an alternative solution. Over a dozen observational studies in critically ill patients suggest that higher protein delivery is beneficial at protecting muscle mass and associated with improved outcomes (decrease in mortality). Not surprisingly, new Society of Critical Care Medicine/American Society for Parenteral and Enteral Nutrition guidelines and expert recommendations suggest higher protein delivery (>1.2 g/kg/d) for critically ill patients. This article provides an introduction to the concepts that delineate the basic principles of modern medical nutrition therapy as it relates to the goal of achieving an optimal management of protein metabolism during critical care illness, highlighting successes achieved so far but also placing significant challenges limiting our success in perspective.