Is There an Association Between Atherosclerotic Burden, Oxidative Stress, and Gut-Derived Lipopolysaccharides?

Could serum zonulin be an intestinal permeability marker in diabetes kidney disease?

“…Non-coeliac gluten sensitivity [ 14 ], inflammatory bowel syndrome [ 15 ], nkylosing spondylitis [ 16 ] and arthritis [ 17 ] also have been linked to changes in intestinal permeability. Besides that, non-communicable diseases, such as obesity [ 18 ] and cardiovascular diseases [ 19 ] were correlated to zonulin levels.…”

LPS-enriched small extracellular vesicles from metabolic syndrome patients trigger endothelial dysfunction by activation of TLR4

“…In line with these findings, mice fed with high-fat diet displayed an increase of low-grade elevation in plasma LPS, which was associated with changes in gut microbiota and permeability, being responsible for the onset of metabolic diseases including increased oxidative stress [32][33][34]. Furthermore, endotoxemia has been proposed to be associated with the development of cardiovascular diseases such as atherosclerosis [35][36][37]. Similar findings have been reported providing evidence that the LPS-TLR4 axis is responsible of metabolic disturbances in obese and diabetic patients [38] in association with an elevation in circulating endotoxin [39] and gut microbiota alterations [40].…”

Gut Microbiota and Atherosclerosis—Focusing on the Plaque Stability

“…Atherosclerosis-prone mice fed with B. vulgatus and B. dorei then showed attenuation of atherosclerotic lesion formation and decrease in gut microbial lipopolysaccharide production. In that circumstance, they discussed that pathogenesis of atherosclerosis alleviation may be due to dampening of systemic innate immune cell activation and Th1-driven inflammation caused by the live Bacteroides treatment-induced reduction in plasma LPS concentration ( 8 ). Loffredo et al have demonstrated that patients with peripheral arterial disease (PAD) have increased systemic LPS concentrations that inversely correlate with the ankle brachial index (ABI) which indicated that LPS can be the promoter of atherosclerotic burden ( 109 ).…”

“…Short-chain fatty acids have already been proven to play protective roles in atherosclerosis, stabilizing plaque ( 5 , 6 ). Simultaneously, they also found that trimethylamine-N-oxide and lipopolysaccharide make the vascular endothelium disorder and plaque unstable and facilitate thrombosis, but the intrinsic mechanism is still not clear ( 7 , 8 ).…”