Betaine hydrochloride is a natural compound found in many foods and also an active methyl-donor which can maintain normal DNA methylation patterns.
It is found that proliferation of HeLa cells is inhibited significantly upon exposure to increasing Betaine hydrochloride levels with the MTT test (p5.0 mg/mL) significantly promotes the apoptosis of HeLa cells (p<0.01). SOD activities of the low dose groups are slightly higher than the control group (p<0.05), and there are obvious synchronicity and correlation among the expression of promoting apoptosis genes Bax, P53, Caspase 3 and apoptosis suppression gene Bcl-2. In response to an apoptosis-inducing stimulus, p53 and cyclin D1 can be activated with blockage of the cell cycle at G1/S or S/G2 checkpoints[1].
Liver-to-body weight ratio is attenuated by Betaine hydrochloride supplementation. When Betaine hydrochloride is added to the alcohol-containing liquid diet, both hepatic triglyceride (TG) accumulation and liver injury are significantly reduced. Betaine hydrochloride supplementation attenuates epididymal fat pad mass loss induced by chronic alcohol feeding. Betaine hydrochloride supplementation prevents the depletion of S-adenosylhomocysteine (SAM) and reduces the increase in S-adenosylhomocysteine (SAH), thereby improving the methylation state of the adipose tissue[2].
References:
[1]. Guo Y, et al. Betaine Effects on Morphology, Proliferation, and p53-induced Apoptosis of HeLa Cervical Carcinoma Cells in Vitro. Asian Pac J Cancer Prev. 2015;16(8):3195-201.
[2]. Dou X, et al. Rectification of impaired adipose tissue methylation status and lipolytic response contributes to hepatoprotective effect of betaine in a mouse model of alcoholic liver disease. Br J Pharmacol. 2014 Sep;171(17):4073-86.