Intakes of sulphur amino acids are implicated in the development of cardiovascular disease because they can affect plasma concentrations of homocysteine. High plasma levels of cystine (oxidised cysteine) and high levels of oxidise glutathione (glutathione disulfide) are associated with cardiovascular disease, possibly because they indicate low antioxidant status. However, the mechanism by which sulphur amino acids are related to cardiovascular disease is not clear, but some evidence suggests that there is temporal variation in plasma levels of cystine, cysteine, glutathione and reduced glutathione in relation to meal frequency and this subsequently has an effect on enzyme, transporter and receptor activities that alter the metabolic milieu. Research has determined that plasma triglycerides are increased in response to a sulphur amino acid free meal, suggesting that amino acid imbalances may cause detectable metabolic changes.
The researchers1 fed 5 males and 3 female subjects (18 to 36 years) a baseline meal that contained adequate dietary sulphur amino acids for 3 days. Following this they were then fed a chemically controlled depletion diet formula that was devoid of sulphur amino acids for 5 days. Finally the subjects were fed an isoenergetic, isonitrogenous diet containing 56mg/kg/d sulphur amino acids for a 4.5 day repletion phase. Plasma samples were collected for up to 8 hours postprandially from the subjects on the first and last day of the depletion and repletion phases of the study, after consumption of 60% of daily calories in one meal. The 1H-NMR spectra indicated that sulphur amino acid depleted food caused changes in a number of metabolic parameters, most notable a rise in plasma triglycerides, and this was confirmed by traditional lipid analysis. In addition there was a plasma rise in the lipoprotein lipase inhibitor apolipoprotein C3 (apoC-III).
These results suggest that imbalances in sulphur amino acid intake can cause metabolic changes that increase risk for cardiovascular disease. Plasma triglycerides increased in this study despite the diets being otherwise equivalent in calories, carbohydrate, fat and nitrogen content. This would indicate that some variable associated with methionine or cysteine is able to alter parameters relating to fat metabolism. The apoC-III protein component of the very low density lipoprotein (VLDL) is a known inhibitor of lipoprotein lipase (present on the capillary walls of adipocytes) and therefore is involved in inhibiting the breakdown of triglycerides and preventing their entry into cells as fatty acids. Sulphur amino acids can affect the surface composition of triglyceride rich lipoproteins (VLDL) through N-methylation of phosphatadylethanolamine which in turn affect the bonding capacity of apoC-III to VLDL. Depletion of sulphur amino acids may therefore raise triglyceride levels by involving rises in ApoC-III concentrations.
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