Interference of altered plasma trace elements profile with hyperhomocysteinemia and oxidative stress damage to insulin secretion dysfunction in Psammomys obesus : focus on the selenium - Université Grenoble Alpes
Article Dans Une Revue Archives of Physiology and Biochemistry Année : 2020

Interference of altered plasma trace elements profile with hyperhomocysteinemia and oxidative stress damage to insulin secretion dysfunction in Psammomys obesus : focus on the selenium

Résumé

The objective of this study is to investigate the relationship between altered plasma trace elements, particularly selenium (Se), with Hyper-homocysteinemia (HhCys) as a predictive factor of insulin secretion dysfunction. The study is carried out on adult Psammomys obesus, divided in 4 experimental groups: (I) Normoglycemic/Normoinsulinemic; (II) Normoglycemic/Hyperinsulinemic; (III) Hyperglycaemic/Hyperinsulinemic and (IV) Hyperglycaemic/Insulin deficiency with ketoacidosis. The data showed that a drastic depletion of Se plasma levels is positively correlated with HhCys (>15 µmol/L; p < .001), concomitantly with decreased GPx activity, GSH levels, and GSH/GSSG ratio in group IV both in plasma and liver. In contrast, SOD activity is increased (p ≤ .001) in group IV both in plasma and liver. However, plasma Cu and Mn levels increased, while plasma Zn levels decreased in group IV (p < .001). Our study confirms the increase of plasma hCys levels seemed to be a major contributing factor to antioxidant capacities and alters the availability of selenium metabolism by interference with homocysteine synthesis in the insulin secretion deficiency stage.
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Dates et versions

hal-04559446 , version 1 (25-04-2024)

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Asma Bouazza, Eric Fontaine, Xavier Leverve, Elhadj-Ahmed Koceir. Interference of altered plasma trace elements profile with hyperhomocysteinemia and oxidative stress damage to insulin secretion dysfunction in Psammomys obesus : focus on the selenium. Archives of Physiology and Biochemistry, 2020, 129 (2), pp.505-518. ⟨10.1080/13813455.2020.1839501⟩. ⟨hal-04559446⟩

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