Obesity

Influence of Obesity and IL-6 on Human Postprandial Amino Acid and Protein Metabolism at Whole-body and Tissue Level

J Clin Endocrinol MetabPublished Nonrandomised controlled trial

Authors' conclusion

Obesity impairs meal-induced muscle-protein gain, through insufficient suppression of protein degradation. Basal IL-6 activity does not regulate muscle protein turnover but influences amino acid metabolism and protein synthesis in extramuscular tissues.

Study context

Population
Men with healthy weight or obesity
Comparison
IL-6 receptor blockade with tocilizumab (3 weeks) vs placebo, in men with healthy weight or obesity
  • Healthy weightn = 12reference
  • Obesityn = 12
Outcome
Amino acid and protein turnover (whole-body, skeletal muscle, subcutaneous adipose tissue), fasted and postprandial
Methodological detailsplacebo-controlled, nonrandomized, participant-blinded, prespecified exploratory outcomes, Trial originally designed to examine IL-6 effects on fat storage (reported previously)
  • Placebo-controlled
  • Nonrandomized
  • Participant-blinded
  • Prespecified exploratory outcomes
  • Trial originally designed to examine IL-6 effects on fat storage (reported previously)

Main finding

As reported in the abstract

  • Obesity was associated with reduced meal-induced muscle-protein gain driven by impaired suppression of muscle protein degradation
  • Obesity was associated with reduced appearance of amino acids from meals
  • In both groups, IL-6 receptor blockade increased fasting and postprandial plasma amino acids
  • In both groups, IL-6 receptor blockade reduced postprandial plasma protein synthesis without affecting skeletal muscle protein turnover
  • In healthy weight group, IL-6 receptor blockade increased amino acid appearance from the meal and postprandial phenylalanine oxidation
  • Prespecified exploratory outcomes

Original publication

Influence of Obesity and IL-6 on Human Postprandial Amino Acid and Protein Metabolism at Whole-body and Tissue Level. J Clin Endocrinol Metab. Published 9 October 2025. doi:10.1210/clinem/dgaf547

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