Abstract
Caloric restriction is one of the most efficient ways to promote weight loss and is known to activate protective metabolic pathways. Frequently reported with weight loss is the undesirable consequence of fat free (lean muscle) mass loss. Weight loss diets with increased dietary protein intake are popular and may provide additional benefits through preservation of fat free mass compared to a standard protein, high carbohydrate diet. However, the precise mechanism by which a high protein diet may mitigate dietary weight loss induced reductions in fat free mass has not been fully elucidated. Maintenance of fat free mass is dependent upon nutrient stimulation of protein synthesis via the mTOR complex, although during caloric restriction a decrease (atrophy) in skeletal muscle may be driven by a homeostatic shift favouring protein catabolism. This review evaluates the relationship between the macronutrient composition of calorie restricted diets and weight loss using metabolic indicators. Specifically we evaluate the effect of increased dietary protein intake and caloric restricted diets on gene expression in skeletal muscle, particularly focusing on biosynthesis, degradation and the expression of genes in the ubiquitin-proteosome (UPP) and mTOR signaling pathways, including MuRF-1, MAFbx/atrogin-1, mTORC1, and S6K1.
Highlights
Current primary treatment strategies for obesity (BMI ≥30 kg/m2) are to consume a low-fat (
Amino acids initiate activation of a cascade of protein and lipid kinases resulting in enhanced mammalian target of rapamycin (mTOR) activity, facilitating the phosphorylation of S6 kinase 1 (S6K1) and hyper-phosphorylation of 4E-BP, resulting in enhanced availability of eIF4E for binding eIF4G and forming an active eIF4F complex resulting in increased protein synthesis [adapted from Layman [88], Anthony et al [89], Drummond et al [61], Um et al [98] and Kimball [90,93] and B; our proposed mechanism whereby high protein calorie restricted weight loss increases Insulin-like growth factor 1 (IGF-1) activating the Phosphatidylinositol 3-kinase/Akt (PI3K)/Serine/threonine protein kinase (Akt) pathway, thereby phosphorylating (P) FoxO transcription factors and downregulating the expression of E3 enzymes atrogin-1 and muscle-specific RING finger protein 1 (MuRF-1), leading to a reduction in protein degradation in skeletal muscle cells
Others have found no alteration of protein levels of Insulin receptor substrate 1 (IRS-1), mTOR or p70S6K in obese and type 2 diabetes mellitus (DM) skeletal muscle compared to age-matched lean participants, a reduction in mTOR phosphorylation in obese and type 2 DM groups and reduced System L transporters, amino acid transporter/solute carrier family 43, member 2 (LAT4) and solute carrier family 3-activator of dibasic and neutral amino acid transport, member 2 (CD98hc) in the type 2 DM group have been reported [64]
Summary
Current primary treatment strategies for obesity (BMI ≥30 kg/m2) are to consume a low-fat (
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