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Cardiovascular disease (CVD) is the predominant cause for morbidity and mortality in diabetes mellitus (DM). Patients with diabetes mellitus have two to three times the incidence of atherosclerotic disease compared to the general population (Kannel & McGee, 1979). Several etiologic factors increase susceptibility to CVD in DM including insulin resistance, dyslipidemia, endothelial dysfunction, prothrombosis, and increased protein glycation (Baynes & Thorpe, 1999). Plasma homocysteine levels are elevated in patients with diabetes, particularly in patients with type 2 diabetes as well as in individuals in prediabetic states who exhibit insulin resistance. Homocysteine (Hcy) is a non-essential amino acid that is produced from demethylation of methionine. Hcy can be remethylated into methionine by means of vitamin B12-dependent methionine synthase and 5-methyltetrahydrofolate as a methyl donor. Hcy can be also catabolized into cysteine (the transsulfuration pathway) via cystathionine beta synthase and cystathioninase, both enzymes being vitamin B6dependent. A third way to remove Hcy is conversion to S-adenosylhomocysteine (SAH). The last reaction is mediated by SAH-hydrolase and favors the SAH formation in case of increased Hcy concentrations. S-Adenosyl methionine (SAM) is a universal methyl donor that is formed from methionine and converted into SAH after donating its methyl group. SAH is a potent inhibitor of most known methyltransferases (Kloor & Osswald, 2004). Among the main determinants of tHcy levels in non-diabetic subjects are age, sex, renal function, several diseases, drugs, coffee and chronic alcohol consumption, smoking and physical inactivity (Refsum et al., 2006). Genetic factors and nutritional deficiencies of folate

Interactions Between Total Plasma Homocysteine, Oxidized LDL Levels, Thiolactonase Activities and Dietary Habits in Tunisian Diabetic Patients