Abstract

Homocysteine (Hcy) is a critical indicator of cardiovascular disease. High levels of Hcy have now been recognised as a risk factor for the development of a wide range of diseases. Hyperhomocysteinemia (Hhcy) can be induced by methionine or Hcy supplementation. On the other hand, Glutathione (GSH) is a major antioxidant in the body and also an important compound for oxidative defence. It is composed of 3 amino acids: cysteine, glutamate, and glycine. Interestingly, methionine is also a crucial compound in GSH synthesis. This study aims to assess the impact of 1% L-methionine feeding (10 or 30 weeks) on the body weight and serum Hcy and GSH levels of young adult (16 weeks) and middle-aged (36 weeks) Wistar rats of both sexes. Serum was analysed for Hcy and reduced GSH levels by liquid chromatography mass spectrometry (LCMS) in response to 1% L-methionine feeding. One percent L-methionine feeding decreased body weight in all conditions investigated, although this only reached significance in males after 10 weeks supplementation and females after 30 weeks supplementation. It also induced a significant increase in the serum Hcy levels of male Wistar rats, whilst having no significant effect on Hcy serum levels in female rats. Finally, we also observed a small increase in serum GSH levels in female Wistar rats but no change in serum GSH levels in the males. These results suggest that methionine feeding affects body weight homeostasis and alters by products of methionine catabolism.

Highlights

  • Elevated concentrations of serum homocysteine (Hcy) have recently been shown to be a high risk factor for cardiovascular diseases [1]

  • Hcy is biosynthesised during methionine metabolism [2,3]

  • Common causes for Hhcy are: renal disease [10], insufficiency of vitamins contributing to Hcy metabolism [11], excess amount of dietary methionine [12,13] and deficit of enzymes involved in Hcy metabolism [3]

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Summary

Introduction

Elevated concentrations of serum homocysteine (Hcy) have recently been shown to be a high risk factor for cardiovascular diseases [1]. Hcy is biosynthesised during methionine metabolism [2,3]. A disturbance in the Hcy metabolic pathway causes Hcy accumulation leading to Hyperhomocysteinemia (Hhcy) [7,8,9]. Common causes for Hhcy are: renal disease [10], insufficiency of vitamins contributing to Hcy metabolism [11], excess amount of dietary methionine [12,13] and deficit of enzymes involved in Hcy metabolism [3]. It has been reported that in atherosclerotic patients with high levels of cholesterol, there was a considerable elevation in plasma Hcy concentrations [14]

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