Glycine ameliorates liver injury and vitamin D deficiency induced by bile duct ligation

Abstract

Background: Patients with chronic liver disease had lower serum concentrations 25-hydroxyvitamin D (25OHD). Glycine, a nonessential amino acid, exerts anti-inflammatory, cytoprotective, and immunomodulatory properties. This study aimed to establish a tandem mass spectrometry assay to measure 25OHD in guinea pigs serum and to investigate the effects of glycine against the liver damage induced by bile duct ligation (BDL).

Methods: BDL was performed on male guinea pigs. Glycine, alanine, serine or tyrosine was given by intraperitoneal injection. The animals were sacrificed and examined at 7 and 14 days after BDL. Serum concentrations of total bilirubin and aminotransferase were measured. Serum concentrations of 25OHD2 and 25OHD3 were measured by API 5000 mass spectrometer. In addition, oxidative stress was assessed by serum ischemia-modified albumin (IMA) and hepatic malondialdehyde (MDA), and apoptosis by hepatic caspase 3 activities.

Results: Serum 25OHD concentrations were decreased around 50% in the BDL group at days 7 and 14 post ligation, compared to sham (mean 65.3 ng/ml, p<0.005). Glycine but not other amino acid treatment blunted the reduced serum 25OHD (52.6 ng/ml, p<0.05) resulting from BDL. The concentrations of 25OHD were negatively associated with concentrations of IMA (r=-0.305, p<0.05) and caspase 3 (r=-0.562, p<0.0001). At day-14 post ligation, glycine treatment also ameliorated liver damage indicated by serum AST (p<0.005), ALT (p<0.05) and hepatic caspase 3 activities (p<0.05) and oxidative stress.

Conclusion: Our results indicate that glycine may protect against BDL-induced liver injury through attenuation of oxidative stress, apoptosis and the vitamin D deficiency.