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<p>β-Alanine is a non-essential β-amino acid used as a dietary supplement for improvement of exercise performance. The hepatic influence of β-alanine has been controversial in previous studies and its effects on nonalcoholic fatty liver disease (NAFLD) are uncertain. In the present study, we examined the role of β-alanine on diet-induced NAFLD in mice and determined the hepatic S-amino acid (SAA) metabolism to identify the cellular mechanisms. Male C57BL/6 mice were provided with a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) for 2&#xa0;weeks to induce NAFLD, and simultaneously supplemented with β-alanine (3%, w/v) in drinking water. CDAHFD-induced liver injury, steatosis, and oxidative stress as shown by the increased serum alanine aminotransferase and aspartate aminotransferase activities, and hepatic triglyceride and lipid peroxide levels, respectively, but β-alanine alleviated these changes. The CDAHFD promoted significant changes in SAA metabolites, including reduced S-adenosylmethionine (SAM) and hypotaurine levels, and elevated homocysteine and taurine levels in the liver. β-Alanine attenuated the decrement of the SAM induced by the CDAHFD via the restoration of methionine adenosyltransferase activity, which appeared to ameliorate fat accumulation by stimulating hepatic lipid export via very-low-density lipoprotein secretion. Moreover, the induction of fatty acid β-oxidation, as shown by the elevations of peroxisome proliferator-activated receptor-gamma coactivator 1-α, carnitine palmitoyltransferase 1A, and acyl-CoA dehydrogenase medium chain proteins, may contribute to the anti-steatogenic effect of β-alanine. Normalizations of hepatic homocysteine and hypotaurine levels due to the restorations of cystathionine β-synthase and cysteine sulfinic acid decarboxylase, respectively, along with increased glutathione levels may be the mechanisms of inhibition of CDAHFD-induced oxidative stress by β-alanine. These results suggest that β-alanine can improve NAFLD via its antioxidant and anti-steatotic effects by restoring hepatic SAA metabolism.</p>

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β-Alanine alleviated non-alcoholic fatty liver disease via regulation of hepatic sulfur-amino acid metabolism in mice

  • 期刊论文

  • 发表日期：

    2025年9月16日

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  • Joohee Lee,
  • Sou-Hyun Kim,
  • Jiwon Hwang,
  • Young-Suk Jung,
  • Doyoung Kwon

摘要

β-Alanine is a non-essential β-amino acid used as a dietary supplement for improvement of exercise performance. The hepatic influence of β-alanine has been controversial in previous studies and its effects on nonalcoholic fatty liver disease (NAFLD) are uncertain. In the present study, we examined the role of β-alanine on diet-induced NAFLD in mice and determined the hepatic S-amino acid (SAA) metabolism to identify the cellular mechanisms. Male C57BL/6 mice were provided with a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) for 2 weeks to induce NAFLD, and simultaneously supplemented with β-alanine (3%, w/v) in drinking water. CDAHFD-induced liver injury, steatosis, and oxidative stress as shown by the increased serum alanine aminotransferase and aspartate aminotransferase activities, and hepatic triglyceride and lipid peroxide levels, respectively, but β-alanine alleviated these changes. The CDAHFD promoted significant changes in SAA metabolites, including reduced S-adenosylmethionine (SAM) and hypotaurine levels, and elevated homocysteine and taurine levels in the liver. β-Alanine attenuated the decrement of the SAM induced by the CDAHFD via the restoration of methionine adenosyltransferase activity, which appeared to ameliorate fat accumulation by stimulating hepatic lipid export via very-low-density lipoprotein secretion. Moreover, the induction of fatty acid β-oxidation, as shown by the elevations of peroxisome proliferator-activated receptor-gamma coactivator 1-α, carnitine palmitoyltransferase 1A, and acyl-CoA dehydrogenase medium chain proteins, may contribute to the anti-steatogenic effect of β-alanine. Normalizations of hepatic homocysteine and hypotaurine levels due to the restorations of cystathionine β-synthase and cysteine sulfinic acid decarboxylase, respectively, along with increased glutathione levels may be the mechanisms of inhibition of CDAHFD-induced oxidative stress by β-alanine. These results suggest that β-alanine can improve NAFLD via its antioxidant and anti-steatotic effects by restoring hepatic SAA metabolism.