Interleukin-1beta may act on hepatocytes to boost plasma homocysteine – The increased cardiovascular risk associated with elevated homocysteine may be mediated by this cytokine
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-1beta can act on hepatocytes to suppress expressi...
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| Published in | Medical hypotheses Vol. 102; pp. 78 - 81 |
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| Main Authors | , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Ltd
01.05.2017
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0306-9877 1532-2777 1532-2777 |
| DOI | 10.1016/j.mehy.2017.03.022 |
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| Abstract | 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-1beta 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-1beta (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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| AbstractList | 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-1beta 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-1beta (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. 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-1beta 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-1beta (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.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-1beta 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-1beta (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. Abstract 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-1beta 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-1beta (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. |
| Author | McCarty, Mark F. DiNicolantonio, James J. O'Keefe, James H. |
| Author_xml | – sequence: 1 givenname: Mark F. surname: McCarty fullname: McCarty, Mark F. email: markfmccarty@gmail.com organization: Catalytic Longevity, Carlsbad, CA, USA – sequence: 2 givenname: James H. surname: O'Keefe fullname: O'Keefe, James H. email: jokeefe@saint-lukes.org organization: Saint Luke’s Mid America Heart Institute, Kansas City, USA – sequence: 3 givenname: James J. surname: DiNicolantonio fullname: DiNicolantonio, James J. email: jjdinicol@gmail.com organization: Saint Luke’s Mid America Heart Institute, Kansas City, USA |
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| Keywords | CRP C-reactive protein Cardiovascular CAD Low Density Lipoprotein Interleukin-1beta Rosuvastatin IL-1β Coronary Artery Disease IL-6 Interleukin-6 CV CBS LDL Homocysteine SAM cardiovascular interleukin-1beta S-adenosylmethionine interleukin-6 cystathionine beta-synthase |
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| SubjectTerms | Animals C-reactive protein Cardiovascular Coronary Artery Disease Coronary Artery Disease - blood Coronary Artery Disease - immunology Evidence-Based Medicine Homocysteine Homocysteine - blood Homocysteine - immunology Humans Immunologic Factors - immunology Inflammation Mediators - immunology Interleukin-1beta Interleukin-1beta - immunology Interleukin-6 Internal Medicine Low Density Lipoprotein Models, Cardiovascular Models, Immunological Peptide Fragments - immunology Rosuvastatin |
| Title | Interleukin-1beta may act on hepatocytes to boost plasma homocysteine – The increased cardiovascular risk associated with elevated homocysteine may be mediated by this cytokine |
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