(S)-b-aminoisobutyric acid is a non-protein amino acid produced through the catabolism of thymine and valine[1]. (S)-b-aminoisobutyric acid plays a key role in energy metabolism, fatty acid oxidation, and muscle metabolism, and is commonly used in research on cardioprotection, body weight, and energy balance[2,3,4].
In vitro, treatment of H9C2 cardiomyocytes with (S)-b-aminoisobutyric acid (10, 20, 30μM) for 24h concentration-dependently increased the phosphorylation levels of AMP-activated protein kinase (AMPK). (S)-b-aminoisobutyric acid (30μM) treatment of H9C2 cardiomyocytes for 24h significantly restored the reduction in ATP production induced by H2O2[5]. Treatment of bone marrow-derived macrophages (BMMs) with (S)-b-aminoisobutyric acid (60μM) during the early (days 0-2) or middle (days 2-4) stages of osteoclast induction significantly inhibited the formation of TRAP-positive multinucleated cells, whereas treatment during the late stage (days 4-6) showed a weaker inhibitory effect[6].
In vivo, oral administration of (S)-b-aminoisobutyric acid (75 mg/kg/day) by gavage to Sprague-Dawley rats with heart failure (HF) for 8 weeks significantly reduced cardiomyocyte apoptosis (decreased number of TUNEL-positive cells)[5]. Pretreatment of C57BL/6 mice with (S)-b-aminoisobutyric acid (150mg/kg/day) by gavage for 10 days, followed by the establishment of a lung ischemia-reperfusion (I/R) injury model, significantly increased the nuclear translocation of Nrf-2 in the lung tissue of mice with I/R injury[7].
References:
[1] CRUMPLER H R, DENT C E, HARRIS H, et al. β-Aminoisobutyric acid (α-methyl-β-alanine): a new amino-acid obtained from human urine[J]. 1951.
[2] BEGRICHE K, MASSART J, ABBEY‐TOBY A, et al. β‐Aminoisobutyric acid prevents diet‐induced obesity in mice with partial leptin deficiency[J]. Obesity, 2008, 16(9): 2053-2067.
[3] STAUTEMAS J, VAN KUILENBURG A B P, STROOMER L, et al. Acute aerobic exercise leads to increased plasma levels of R-and S-β-aminoisobutyric acid in humans[J]. Frontiers in Physiology, 2019, 10: 1240.
[4] VALLEJO J A, KITASE Y, GANESH T, et al. L-β-aminoisobutyric acid (L-BAIBA) in combination with voluntary wheel running exercise enhances musculoskeletal properties in middle-age male mice[J]. Aging (Albany NY), 2025, 17(10): 2475.
[5] YU Y, CHEN W, YU M, et al. Exercise-generated β-aminoisobutyric acid (BAIBA) reduces cardiomyocyte metabolic stress and apoptosis caused by mitochondrial dysfunction through the miR-208b/AMPK pathway[J]. Frontiers in Cardiovascular Medicine, 2022, 9: 803510.
[6] HUANG Z W, YU Y P, HE X R, et al. Exercise suppresses osteoclastogenesis by increasing the secretion of muscle-derived L-β-aminoisobutyric acid[J]. Journal of Sport and Health Science, 2025: 101077.
[7] ZHANG Z, LI X, GUO J, et al. β-aminoisobutyrics acid, a metabolite of BCAA, activates the AMPK/Nrf-2 pathway to prevent ferroptosis and ameliorates lung ischemia-reperfusion injury[J]. Molecular Medicine, 2023, 29(1): 164.
(S)-b-aminoisobutyric acid是一种经胸腺嘧啶和缬氨酸分解代谢产生的非蛋白质氨基酸[1]。(S)-b-aminoisobutyric acid在能量代谢、脂肪酸氧化和肌肉代谢中起关键作用，通常用于心脏保护、体重和能量平衡的研究[2,3,4]。
在体外，(S)-b-aminoisobutyric acid（10, 20, 30μM）处理H9C2心肌细胞24h，浓度依赖性地增加了AMP激活蛋白激酶（AMPK）的磷酸化水平。(S)-b-aminoisobutyric acid（30μM）处理H9C2心肌细胞24h，显著恢复了由H2O2引起的ATP生成减少[5]。(S)-b-aminoisobutyric acid（60μM）在诱导破骨分化的早期（0-2天）或中期（2-4天）处理骨髓来源巨噬细胞BMMs，可显著抑制TRAP阳性多核细胞的形成，而在晚期（4-6天）处理则抑制作用较弱[6]。
在体内，(S)-b-aminoisobutyric acid（75mg/kg/day）通过口服灌胃处理心力衰竭（HF）的Sprague-Dawley大鼠8周，显著减少了心肌细胞凋亡（TUNEL阳性细胞减少）[5]。(S)-b-aminoisobutyric acid（150mg/kg/day）通过灌胃预处理C57BL/6小鼠10天，后建立肺缺血再灌注（I/R）损伤模型，可显著增加I/R损伤小鼠肺组织中Nrf-2的核内易位[7]。