Insulin does not stimulate β-alanine transport into human skeletal muscle

Author:

Gonçalves Lívia de Souza1,Kratz Caroline1,Santos Lívia2,Carvalho Victor Henrique3,Sales Lucas Peixoto1,Nemezio Kleiner1,Longobardi Igor1,Riani Luiz Augusto1,Lima Marcelo Miranda de Oliveira4,Saito Tiemi1,Fernandes Alan Lins1,Rodrigues Joice3,James Ruth Margaret2,Sale Craig2ORCID,Gualano Bruno1,Geloneze Bruno4,de Medeiros Marisa Helena Gennari3,Artioli Guilherme Giannini1

Affiliation:

1. Applied Physiology and Nutrition Research Group; School of Physical Education and Sport, Rheumatology Division, Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, Brazil

2. Musculoskeletal Physiology Research Group, Sport, Health, and Performance Enhancement Research Centre, Nottingham Trent University, Nottingham, United Kingdom

3. Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, Brazil

4. Laboratory of Investigation in Metabolism and Diabetes (LIMED)/Gastrocentro Departamento de Cirurgia, Universidade de Campinas (UNICAMP), Campinas, Brazil

Abstract

To test whether high circulating insulin concentrations influence the transport of β-alanine into skeletal muscle at either saturating or subsaturating β-alanine concentrations, we conducted two experiments whereby β-alanine and insulin concentrations were controlled. In experiment 1, 12 men received supraphysiological amounts of β-alanine intravenously (0.11 g·kg−1·min−1for 150 min), with or without insulin infusion. β-Alanine and carnosine were measured in muscle before and 30 min after infusion. Blood samples were taken throughout the infusion protocol for plasma insulin and β-alanine analyses. β-Alanine content in 24-h urine was assessed. In experiment 2, six men ingested typical doses of β-alanine (10 mg/kg) before insulin infusion or no infusion. β-Alanine was assessed in muscle before and 120 min following ingestion. In experiment 1, no differences between conditions were shown for plasma β-alanine, muscle β-alanine, muscle carnosine and urinary β-alanine concentrations (all P > 0.05). In experiment 2, no differences between conditions were shown for plasma β-alanine or muscle β-alanine concentrations (all P > 0.05). Hyperinsulinemia did not increase β-alanine uptake by skeletal muscle cells, neither when substrate concentrations exceed the Vmaxof β-alanine transporter TauT nor when it was below saturation. These results suggest that increasing insulin concentration is not necessary to maximize β-alanine transport into muscle following β-alanine intake.

Publisher

American Physiological Society

Subject

Cell Biology,Physiology

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