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Article Publish Status: FREE
Abstract Title:

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

Abstract Source:

Nutrients. 2022 Feb 8 ;14(3). Epub 2022 Feb 8. PMID: 35277077

Abstract Author(s):

Xin Dai, Si Liu, Lokyu Cheng, Ting Huang, Honghui Guo, Dongliang Wang, Min Xia, Wenhua Ling, Yunjun Xiao

Article Affiliation:

Xin Dai

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/SAHHmice. 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/SAHHmice, 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/SAHHmice. 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.

Study Type : Animal Study

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