Homocysteine is that blood-borne amino-acid that degenerates vascular
systems & is involved in the pathogenesis of cardio-vascular diseases.
It is also involved in the re-methylation process back to methionine.
C-Reactive Protein (C-RP) is a strong inflammatory marker that
underscores the atherosclerotic process. Is there a direct metabolic
link between homocysteine & C-RP? If so. HOW does it work?

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Clarification of Question by ngang-ga on 02 Jun 2003 16:50 PDT

I know the work of Yudkin et al [C-RP protein in healthy subjects:
Associations with obesity, insulin resistance, & endothelial
dysfunction. In “Arterioscler. Thromb. Vasc. Biol. ’99; 19: 972-978]
showed a positive association of C-RP, TNF-alpha & IL-6 concentrations
with measures of: obesity, extent of central fat distribution (greater
correlative index than overall, systemic obesity), and insulin
resistance. As well, Hotamisligil et (’95) & Purhoit et al (’95)
showed that adipose tissue is an important source of TNF-a & IL-6, AND
Baumann et al (’94) and Papanicolaou et al (’98) showed that these
cytokines are the main regulators of C-RP production.

Does the afore-going somewhat imply that there is a strong, positive
correlation between central abdominal obesity & insulin resistance
WITH homocysteine (a methylation mediator & precursor of the
athero-toxic homocystine) IF there is, indeed, a metabolic connection
between homocysteine & C-RP?