Anabolic sensitivity of postprandial muscle protein synthesis to the ingestion of a protein-dense food is reduced in overweight and obese young adults.

Journal Article

Background

Excess body fat diminishes muscle protein synthesis rates in response to hyperinsulinemic-hyperaminoacidemic clamps. However, muscle protein synthetic responses after the ingestion of a protein-dense food source across a range of body mass indexes (BMIs) have not been compared.

Objective

We compared the myofibrillar protein synthetic response and underlying nutrient-sensing mechanisms after the ingestion of lean pork between obese, overweight, and healthy-weight adults.

Design

Ten healthy-weight [HW; BMI (in kg/m2 ): 22.7 ± 0.4], 10 overweight (OW; BMI: 27.1 ± 0.5), and 10 obese (OB; BMI: 35.9 ± 1.3) adults received primed continuous l-[ring-13 C6 ]phenylalanine infusions. Blood and muscle biopsy samples were collected before and after the ingestion of 170 g pork (36 g protein and 3 g fat) to assess skeletal muscle anabolic signaling, amino acid transporters [large neutral and small neutral amino acid transporters (LAT1, SNAT2) and CD98], and myofibrillar protein synthesis.

Results

At baseline, OW and OB groups showed greater relative amounts of mammalian target of rapamycin complex 1 (mTORC1) protein than the HW group. Pork ingestion increased mTORC1 phosphorylation only in the HW group (P = 0.001). LAT1 and SNAT2 protein content increased during the postprandial period in all groups (time effect, P < 0.05). Basal myofibrillar protein synthetic responses were similar between groups (P = 0.43). However, myofibrillar protein synthetic responses (0-300 min) were greater in the HW group (1.6-fold; P = 0.005) after pork ingestion than in the OW and OB groups.

Conclusions

There is a diminished myofibrillar protein synthetic response to the ingestion of protein-dense food in overweight and obese adults compared with healthy-weight controls. These data indicate that impaired postprandial myofibrillar protein synthetic response may be an early defect with increasing fat mass, potentially dependent on altered anabolic signals, that reduces muscle sensitivity to food ingestion. This trial was registered at clinicaltrials.gov as NCT02613767.

Full Text

Duke Authors

Cited Authors

  • Beals, JW; Sukiennik, RA; Nallabelli, J; Emmons, RS; van Vliet, S; Young, JR; Ulanov, AV; Li, Z; Paluska, SA; De Lisio, M; Burd, NA

Published Date

  • October 2016

Published In

Volume / Issue

  • 104 / 4

Start / End Page

  • 1014 - 1022

PubMed ID

  • 27604771

Pubmed Central ID

  • 27604771

Electronic International Standard Serial Number (EISSN)

  • 1938-3207

International Standard Serial Number (ISSN)

  • 0002-9165

Digital Object Identifier (DOI)

  • 10.3945/ajcn.116.130385

Language

  • eng