Protein-rich food ingestion stimulates mitochondrial protein synthesis in sedentary young adults of different BMIs

TY - JOUR

T1 - Protein-rich food ingestion stimulates mitochondrial protein synthesis in sedentary young adults of different BMIs

AU - Mackenzie, Richard

PY - 2017/6/29

Y1 - 2017/6/29

N2 - AbstractContextExcess 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.ObjectiveWe 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).MethodsTen 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.ResultsPork 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).ConclusionsProtein-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.© 2017, Endocrine Society. The attached document (embargoed until 29/06/18) is an author produced version of a paper uploaded in accordance with the publisher’s self- archiving policy. The final published version (version of record) is available online at the link below. Some minor differences between this version and the final published version may remain. We suggest you refer to the final published version should you wish to cite from it.

AB - AbstractContextExcess 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.ObjectiveWe 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).MethodsTen 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.ResultsPork 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).ConclusionsProtein-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.© 2017, Endocrine Society. The attached document (embargoed until 29/06/18) is an author produced version of a paper uploaded in accordance with the publisher’s self- archiving policy. The final published version (version of record) is available online at the link below. Some minor differences between this version and the final published version may remain. We suggest you refer to the final published version should you wish to cite from it.

KW - Obesity

KW - Insulin Resistance

KW - Diabetes Mellitus, Type 2

U2 - 10.1210/jc.2017-00360

DO - 10.1210/jc.2017-00360

M3 - Article

SN - 0021-972X

VL - 102

SP - 3415

JO - The Journal of clinical endocrinology and metabolism

JF - The Journal of clinical endocrinology and metabolism

IS - 9

ER -