Atherosclerosis
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In recent years, a number of studies have alluded to the importance of the intestinal microflora in controlling whole-body metabolic homeostasis and organ physiology. In particular, it has been suggested that the hepatic production of trimethylamine-N-oxide (TMAO) from gut microbiota-derived trimethylamine (TMA) may enhance cardiovascular risk via promoting atherosclerotic lesion development. The source of TMA production via the gut microbiota appears to originate from 2 principle sources, either phosphatidylcholine/choline and/or L-carnitine. ⋯ In contrast, a number of studies demonstrate beneficial properties for l-carnitine consumption against metabolic diseases including skeletal muscle insulin resistance and ischemic heart disease. Furthermore, fish are a significant source of TMAO, but dietary fish consumption and fish oil supplementation may exhibit positive effects on cardiovascular health. In this mini-review we will discuss the discrepancies regarding L-carnitine supplementation and its possible negative effects on cardiovascular risk through potential increases in TMAO production, as well as its positive effects on metabolic health via increasing glucose metabolism in the muscle and heart.
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We examined the association between the ratio of serum eicosapentaenoic acid to arachidonic acid (EPA/AA) or the docosahexaenoic acid (DHA)/AA and the development of cardiovascular disease in a general Japanese population. ⋯ Our findings suggest that a lower serum EPA/AA ratio is associated with a greater risk of cardiovascular disease, especially coronary heart disease, among subjects with higher HS-CRP levels in the general Japanese population.
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Dual specificity phosphatase 1 (DUSP1) inhibits mitogen activated protein kinase activity, and is activated by several stimuli such as sustained hypoxia, oxidative stress, and hormones. However, the effect of intermittent hypoxia is not known. The aim of this study was to evaluate the role of intermittent hypoxia on DUSP1 expression, and to validate its role in a human model of intermittent hypoxia, as seen in obstructive sleep apnea (OSA). OSA is characterized by recurrent episodes of hypoxemia/reoxygenation and is a known risk factor for cardiovascular morbidity. ⋯ Intermittent hypoxia increases MnSOD activity via increased DUSP1 expression in HCAEC. Similarly, overnight intermittent hypoxemia in patients with OSA induces expression of DUSP1, which may mediate increases of MnSOD expression and activity. This may contribute significantly to neutralizing the effects of reactive oxygen species, a consequence of the intermittent hypoxemia/reperfusion elicited by OSA.