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Homocysteine as a non-classical risk factor for atherosclerosis in relation to pharmacotherapy of type 2 diabetes mellitus.

Homocysteine as a non-classical risk factor for atherosclerosis in relation to pharmacotherapy of type 2 diabetes mellitus.
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Borowska M, Dworacka M, Winiarska H, Krzyżagórska E,


Borowska M, Dworacka M, Winiarska H, Krzyżagórska E, (click to view)

Borowska M, Dworacka M, Winiarska H, Krzyżagórska E,

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Acta biochimica Polonica 2017 12 07() doi 10.18388/abp.2016_1489
Abstract
AIMS
The aim of our study was to evaluate which of the pharmacotherapeutic methods that are frequently used to treat type 2 diabetes is associated with the most beneficial profile in relation to pro-atherogenic homocysteine levels.

PATIENTS AND METHODS
We measured the serum homocysteine level in 182 patients with type 2 diabetes treated with metformin (89), treated with insulin in combination with metformin (31), receiving sulfonylureas (31) and treated conventionally with insulin (31). The total homocysteine levels in the serum were assayed. To exclude the influence of selected metabolic and anthropometric factors on the differences between the examined groups, multivariate analysis of covariance was used (ANCOVA). In this analysis, serum homocysteine concentration was the dependent variable, while diabetes duration, waist circumference, HbA1c, 1,5-anhydro-D-glucitol, fasting glycaemia and peptide C were used as covariates.

RESULTS
The serum homocysteine levels in patients treated with insulin in monotherapy were significantly higher than what was observed in the metformin treated subjects and in the patients receiving insulin combined with metformin. The analysis of covariance also confirmed that the differences between the therapeutic groups were affected by waist circumference and the C-peptide levels.

CONCLUSION
We conclude that conventional insulin therapy may have a negative effect on pro-atherogenic homocysteine levels in patients with type 2 diabetes. This study revealed that pro-atherogenic homocysteine levels may not only be modified by pharmacotherapy of type 2 diabetes, but also by beta cell secretory function and abdominal obesity.

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