» Articles » PMID: 35277077

Betaine Supplementation Attenuates S-Adenosylhomocysteine Hydrolase-Deficiency-Accelerated Atherosclerosis in Apolipoprotein E-Deficient Mice

Overview
Journal Nutrients
Date 2022 Mar 12
PMID 35277077
Authors
Affiliations
Soon will be listed here.
Abstract

S-adenosylhomocysteine (SAH) is a risk factor of cardiovascular diseases and atherosclerosis. However, the causal association between SAH and atherosclerosis is still uncertain. In the present study, heterozygous SAH hydrolase (SAHH) knockout mice were bred with apolipoprotein E-deficient mice to produce ApoE/SAHH mice. At 8 weeks of age, these mice were fed on AIN-93G diets added with or without betaine (4 g betaine/100 g diet) for 8 weeks. Compared with ApoE/SAHH mice, SAHH deficiency caused an accumulation of plasma SAH concentration and a decrease in S-adenosylmethionine (SAM)/SAH ratio as well as plasma homocysteine levels. Betaine supplementation lowered SAH levels and increased SAM/SAH ratio and homocysteine levels in ApoE/SAHH mice. Furthermore, SAHH deficiency promoted the development of atherosclerosis, which was reduced by betaine supplementation. The atheroprotective effects of betaine on SAHH-deficiency-promoted atherosclerosis were associated with inhibition of NFκB inflammation signaling pathway and inhibition of proliferation and migration of smooth muscle cells. In conclusion, our results suggest that betaine supplementation lowered plasma SAH levels and protected against SAHH-deficiency-promoted atherosclerosis through repressing inflammation and proliferation and migration of smooth muscle cells.

Citing Articles

Role of Vanin-1 Gene Methylation in Fat Synthesis in Goose Liver: Effects of Betaine and 5-Azacytidine Treatments.

Wang X, Shao Y, Yang Z, Yang H, Wang Z Animals (Basel). 2025; 15(5).

PMID: 40076002 PMC: 11899362. DOI: 10.3390/ani15050719.


Effect of betaine on growth performance, methionine metabolism, and methyl transfer in broilers aged 1 to 21 days and fed a low-methionine diet.

Wang H, Liu L, He X, Bian G J Poult Sci. 2025; 62:2025010.

PMID: 40060329 PMC: 11879611. DOI: 10.2141/jpsa.2025010.


Catalpol inhibits HHcy-induced EndMT in endothelial cells by modulating ROS/NF-κB signaling.

Wu C, Li Y, Liu S, Wang L, Wang X BMC Cardiovasc Disord. 2024; 24(1):431.

PMID: 39148029 PMC: 11328392. DOI: 10.1186/s12872-024-04046-z.


Transcriptomic-based clustering of human atherosclerotic plaques identifies subgroups with different underlying biology and clinical presentation.

Mokry M, Boltjes A, Slenders L, Bel-Bordes G, Cui K, Brouwer E Nat Cardiovasc Res. 2023; 1(12):1140-1155.

PMID: 37920851 PMC: 10621615. DOI: 10.1038/s44161-022-00171-0.


Hyperhomocysteinemia and Accelerated Aging: The Pathogenic Role of Increased Homocysteine in Atherosclerosis, Osteoporosis, and Neurodegeneration.

Alkaissi H, McFarlane S Cureus. 2023; 15(7):e42259.

PMID: 37605676 PMC: 10440097. DOI: 10.7759/cureus.42259.


References
1.
Ji C, Kaplowitz N . Betaine decreases hyperhomocysteinemia, endoplasmic reticulum stress, and liver injury in alcohol-fed mice. Gastroenterology. 2003; 124(5):1488-99. DOI: 10.1016/s0016-5085(03)00276-2. View

2.
Green T, Skeaff C, McMahon J, Venn B, Williams S, Devlin A . Homocysteine-lowering vitamins do not lower plasma S-adenosylhomocysteine in older people with elevated homocysteine concentrations. Br J Nutr. 2010; 103(11):1629-34. DOI: 10.1017/S0007114509993552. View

3.
Xiao Y, Xia J, Cheng J, Huang H, Zhou Y, Yang X . Inhibition of S-Adenosylhomocysteine Hydrolase Induces Endothelial Dysfunction via Epigenetic Regulation of p66shc-Mediated Oxidative Stress Pathway. Circulation. 2019; 139(19):2260-2277. DOI: 10.1161/CIRCULATIONAHA.118.036336. View

4.
Schwab U, Alfthan G, Aro A, Uusitupa M . Long-term effect of betaine on risk factors associated with the metabolic syndrome in healthy subjects. Eur J Clin Nutr. 2010; 65(1):70-6. DOI: 10.1038/ejcn.2010.230. View

5.
Zhu N, Xiang Y, Zhao X, Cai C, Chen H, Jiang W . Thymoquinone suppresses platelet-derived growth factor-BB-induced vascular smooth muscle cell proliferation, migration and neointimal formation. J Cell Mol Med. 2019; 23(12):8482-8492. PMC: 6850929. DOI: 10.1111/jcmm.14738. View