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Effect of GABA on oxidative stress in the skeletal muscles and plasma free amino acids in mice fed high‐fat diet
Author(s) -
Xie Z.X.,
Xia S.F.,
Qiao Y.,
Shi Y.H.,
Le G.W.
Publication year - 2015
Publication title -
journal of animal physiology and animal nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.651
H-Index - 56
eISSN - 1439-0396
pISSN - 0931-2439
DOI - 10.1111/jpn.12254
Subject(s) - medicine , endocrinology , oxidative stress , chemistry , oxidative phosphorylation , gamma aminobutyric acid , amino acid , metabolism , biochemistry , biology , receptor
Summary Increased levels of plasma free amino acids (p FAA s) can disturb the blood glucose levels in patients with obesity, diabetes mellitus and metabolic syndrome ( MS ) and are associated with enhanced protein oxidation. Oxidation of proteins, especially in the muscles, can promote protein degradation and elevate the levels of p FAA s. Gamma‐aminobutyric acid ( GABA ), a food additive, can reduce high‐fat diet ( HFD )‐induced hyperglycaemia; however, the mechanisms remain unclear. The aim of this study was to evaluate the effects of GABA on protein oxidation and p FAA s changes. One hundred male C 57BL/6 mice were randomly divided into five groups that were fed with control diet, HFD and HFD supplied with 0.2%, 0.12% and 0.06% GABA in drinking water for 20 weeks respectively. HFD feeding led to muscular oxidative stress, protein oxidation, p FAA disorders, hyperglycaemia and augmented plasma GABA levels. Treatment with GABA restored normally fasting blood glucose level and dose‐dependently inhibited body weight gains, muscular oxidation and protein degradation. While medium and low doses of GABA mitigated HFD ‐induced p FAA disorders, the high dose of GABA deteriorated the p FAA disorders. Medium dose of GABA increased the levels of GABA , but high dose of GABA reduced the levels of plasma GABA and increased the activity of succinic semialdehyde dehydrogenase in the liver. Therefore, treatment with GABA mitigated HFD ‐induced hyperglycaemia probably by repairing HFD ‐induced muscular oxidative stress and pFAA disorders in mice. Our data also suggest that an optimal dose of GABA is crucial for the prevention of excess GABA ‐related decrease in the levels of p FAA and GABA as well as obesity.