Interleukin-1beta May Act on Hepatocytes to Boost Plasma Homocysteine – The Increased Cardiovascular Risk Associated with Elevated Homocysteine May be Mediated by this Cytokine

Publication date: Available online 14 March 2017
Source:Medical Hypotheses
Author(s): Mark F McCarty, James H O'Keefe, James J DiNicolantonio
The results of multi-center trials of B vitamin supplementation reveal that, whereas moderately elevated homocysteine predicts increased risk for coronary disease, it does not play a mediating role in this regard. This essay proposes that interleukin 1-beta can act on hepatocytes to suppress expression of the hepatocyte-specific forms of methionine adenosyltransferase; this in turn can be expected to decrease hepatic activity of cystathionine-β-synthase, leading to an increase in plasma homocysteine. It is further proposed that interleukin 1-beta (IL-1β) is a true mediating risk factor for cardiovascular disease, and that elevated homocysteine predicts coronary disease because it can serve as a marker for increased IL-1β activity. Potent statin therapy may decrease IL-1β production by suppressing inflammasome activation – thereby accounting for the marked protection from cardiovascular events observed in the classic JUPITER study, in which the enrolled subjects had low-normal low density lipoprotein cholesterol but elevated C-reactive protein.



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