Protein-Rich Food Ingestion Stimulates Mitochondrial Protein Synthesis in Sedentary Young Adults of Different BMIs

• Published in: The journal of clinical endocrinology and metabolism Vol. 102; no. 9; pp. 3415 - 3424
• Main Authors: Beals, Joseph W, Mackenzie, Richard W A, van Vliet, Stephan, Skinner, Sarah K, Pagni, Brandon A, Niemiro, Grace M, Ulanov, Alexander V, Li, Zhong, Dilger, Anna C, Paluska, Scott A, De Lisio, Michael, Burd, Nicholas A
• Format: Journal Article
• Language: English
• Published: Washington, DC Endocrine Society 01.09.2017; Copyright Oxford University Press; Oxford University Press
• Subjects: Adipose tissue; Adult; Analysis of Variance; Body fat; Body mass; Body Mass Index; Body Weight; Dietary Proteins - administration & dosage; Eating; Female; Food; Glucose; Healthy Volunteers; Humans; Inflammation; Inflammatory diseases; Ingestion; Life Style; Male; Metabolism; Mitochondria; Mitochondrial Proteins - blood; Mitochondrial Proteins - metabolism; Muscle Proteins - metabolism; Muscles; Musculoskeletal diseases; MyD88 protein; Nutrient content; Obesity; Obesity - metabolism; Overweight; Phenylalanine; Pork; Postprandial Period; Protein Biosynthesis; Protein folding; Protein synthesis; Proteins; Red Meat; Reference Values; Sampling Studies; Sedentary behavior; Skeletal muscle; TLR4 protein; Toll-like receptors; Young Adult; Young adults
• ISSN: 0021-972X; 1945-7197
• DOI: 10.1210/jc.2017-00360

Abstract Context Excess fat mass may diminish the anabolic potency of protein-rich food ingestion to stimulate muscle protein subfractional synthetic responses. However, the impact of adiposity on mitochondrial protein synthesis (MPS) rates after protein-rich food ingestion has not been thoroughly examined in vivo in humans. Objective We compared basal and postprandial MPS and markers of muscle inflammation [toll-like receptor 4 (TLR4) and myeloid differentiation primary response protein 88 (MyD88) protein content] in young adults with different body mass indices (BMIs). Methods Ten normal-weight (NW; BMI = 22.7 ± 0.4 kg/m2), 10 overweight (OW; BMI = 27.1 ± 0.5 kg/m2), and 10 obese (OB; BMI = 35.9 ± 1.3 kg/m2) adults received primed continuous L-[ring-13C6]phenylalanine infusions, blood sampling, and skeletal muscle biopsies before and after the ingestion of 170 g of pork. Results Pork ingestion increased muscle TLR4 and MyD88 protein content in the OB group (P < 0.05), but not in the NW or OW groups. Basal MPS was similar between groups (P > 0.05). Pork ingestion stimulated MPS (P < 0.001; 0 to 300 minutes) in the NW (2.5- ± 0.6-fold above baseline values), OW (1.7- ± 0.3-fold), and OB groups (2.4- ± 0.5-fold) with no group differences (P > 0.05). Conclusions Protein-dense food ingestion promotes muscle inflammatory signaling only in OB adults. However, the consumption of a dinner-sized amount of protein strongly stimulated a postprandial MPS response irrespective of BMI. Our data suggest that alterations in postprandial MPS are unlikely to contribute to compromised muscle macronutrient metabolism witnessed with obesity. We studied the interaction of protein dense food ingestion on the stimulation of mitochondrial protein synthesis and found no impairments in the response between young adults of different BMI scores.