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Hyperhomocysteinemia as a component of syndrome X
Mor Oron-Herman1, Talma Rosenthal, Ben-Ami Sela
1Sackler Faculty of Medicine, Tel Aviv University, Israel.
Insights
Syndrome X, characterized by metabolic disorders, was linked to higher homocysteine levels in rats fed a fructose diet. This suggests hyperhomocysteinemia contributes to vascular risk in metabolic syndrome.
Area of Science:
- Metabolic Syndrome Research
- Cardiovascular Disease Risk Factors
Background:
- Syndrome X (metabolic syndrome) involves hyperinsulinemia, hypertriglyceridemia, and hypertension, increasing vascular disease risk.
- Hyperhomocysteinemia is an independent risk factor for cardiovascular and cerebrovascular diseases, often seen in insulin-resistant individuals.
Purpose of the Study:
- To investigate the relationship between Syndrome X and hyperhomocysteinemia using a rat model.
- To determine if dietary factors can induce both conditions simultaneously.
Main Methods:
- Two groups of rats were fed either a fructose-enriched diet or standard chow for 5 weeks.
- Key metabolic markers (insulin, triglycerides, cholesterol) and homocysteine levels were measured, along with systolic blood pressure.
Main Results:
- Fructose diet induced Syndrome X, significantly increasing insulin, triglycerides, and blood pressure.
- Homocysteine levels were 72% higher in the fructose-fed group compared to controls (P<.01).
- Homocysteine showed significant positive correlations with insulin, triglycerides, and systolic blood pressure.
Conclusions:
- Hyperhomocysteinemia is an integral component of this rat model of Syndrome X.
- Findings suggest hyperhomocysteinemia may also be a key factor in human metabolic syndrome, contributing to vascular risk.
Abstract:
Syndrome X, a cluster of several metabolic disorders that includes hyperinsulinemia, hypertriglyceridemia, and hypertension, is associated with severe vascular morbidity. Hyperhomocysteinemia is another risk factor for cardiovascular and cerebrovascular diseases, often exhibited by insulin-resistant patients. In the current study, we investigated the relationship between syndrome X and hyperhomocysteinemia in a rat model. Two groups of rats were fed either fructose-enriched diet or standard rat chow for 5 weeks. Systolic blood pressure (SBP), as well as fasting plasma insulin, triglycerides, total cholesterol, and total homocysteine levels, were determined at the beginning and at the end of the study. A complete metabolic syndrome was induced by the fructose-enriched diet, including hyperinsulinemia, hypertriglyceridemia, and hypertension. Homocysteine concentration was 72% higher after 5 weeks on the fructose diet (8.49 +/- 1.6 v 4.92 +/- 0.9 micromol/l, P<.01). Insulin, triglycerides, SBP, and homocysteine levels were insignificantly changed during 5 weeks on standard rat chow. Homocysteine was positively and significantly correlated with any original component of syndrome X (r=0.565, P=.014 with insulin, r=0.662, P=.001 with triglycerides, and r=0.774, P<.001 with SBP). The results of the present study indicate that hyperhomocysteinemia is an integral component of this rat model of syndrome X. It is thus highly likely that hyperhomocysteinemia is an integral component of the human syndrome X as well, and thereby contributes to the overall high vascular risk associated with this condition.
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