In:
Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 74, No. Suppl_1 ( 2019-09)
Abstract:
Unless there is a genetic defect, most diseases start in our gut. Balance in gut’s microbiome; symbiosis vs dysbiosis need to be maintained during health, however; in diseases such metabolic syndrome, bowl diseases, and hypertension, dysbiosis prevails, but mechanisms are unclear. Our research focuses on homocysteine (Hcy) that occupies a center-stage (Figure). For example, dysbiosis methylate promoters in turn inhibiting genes. Interestingly; product of 1-carbon metabolism is Hcy, unequivocally. Recently, studies on host resistance to antibiotics have shown to be related with inverton-promoter inhibition, presumably because of methylation, thus causing modification promoters by bacterial antigens. These changes force host to lose its drug sensitivity. In this regard, we focus on the role of high methionine diet (HMD, rich in red meat) and measure the effects of a probiotic on cardiac muscle. We employed wild type and hypertensive cystathionine beta synthase (CBS) heterozygote KO mice with and without HMD and with and without a probiotic (PB, Lactobacillus) treatment in drinking water for 16 weeks. Results suggest that matrix metalloproteinase-2 activity was robust in CBS and HMD which was attenuated by PB intervention. Cardiomyocyte contractility and ECHO data suggest mitigation of cardiac dysfunction in CBS and HMD mice with PB. Also, gut microbiota reconstitution resulted in decreased interstitial fibrosis in probiotic mice hearts. Expression of key regenerative factors: DAAM1, DAAM2, REDD1 and BHMT were also improved by PB. In conclusion, our data suggest that probiotic mitigates dysbiotic 1-carbon metabolism induced hypertensive cardiac remodeling.
Type of Medium:
Online Resource
ISSN:
0194-911X
,
1524-4563
DOI:
10.1161/hyp.74.suppl_1.P2009
Language:
English
Publisher:
Ovid Technologies (Wolters Kluwer Health)
Publication Date:
2019
detail.hit.zdb_id:
2094210-2
