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

Journal Article


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.


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).


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.


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).


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.

Full Text

Duke Authors

Cited Authors

  • Beals, JW; Mackenzie, RWA; van Vliet, S; Skinner, SK; Pagni, BA; Niemiro, GM; Ulanov, AV; Li, Z; Dilger, AC; Paluska, SA; De Lisio, M; Burd, NA

Published Date

  • September 2017

Published In

Volume / Issue

  • 102 / 9

Start / End Page

  • 3415 - 3424

PubMed ID

  • 28911136

Pubmed Central ID

  • 28911136

Electronic International Standard Serial Number (EISSN)

  • 1945-7197

International Standard Serial Number (ISSN)

  • 0021-972X

Digital Object Identifier (DOI)

  • 10.1210/jc.2017-00360


  • eng