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Inflammation interferes with the assessment of vitamin A status in magnesium deficiency
Yves Rayssiguier1, Marie-Cécile Alexandre-Gouabau, Bernard Lyan
1INRA, Unité de nutrition humaine, UMR1019, Clermont-Ferrand/Theix, France. yrayssig@clermont.inra.fr
Abstract:
Hyporetinemia is observed in several pathological conditions including a primary deficiency of vitamin A and has also been reported to accompany inflammatory diseases. Experimental magnesium (Mg) deficiency in rodents is accompanied by an inflammatory syndrome. The present study was designed to determine whether the acute phase response in Mg-deficient rats can modify vitamin A status. Clinical symptoms of acute phase response were observed in Mg-deficient rats and were accompanied by a reduction in plasma retinol and of plasma retinol binding protein (RBP). Mg deficiency in rats resulted in hyporetinemia without a significant decrease in liver retinol reserves. Consequently, the data strongly suggest that the decrease in plasma retinol concentration, resulting from the level of its binding protein, is related to the inflammatory effect of Mg deficiency. These results point to the possible interference of Mg deficiency on the use of plasma retinol as an indicator of vitamin A status.
Insights
Magnesium deficiency in rats causes hyporetinemia by reducing plasma retinol binding protein (RBP), not liver vitamin A stores. This suggests Mg deficiency interferes with vitamin A status assessment during inflammation.
Area of Science:
- Biochemistry
- Nutrition Science
- Pathology
Background:
- Hyporetinemia (low plasma retinol) is linked to vitamin A deficiency and inflammatory diseases.
- Experimental magnesium (Mg) deficiency in rodents induces an inflammatory syndrome.
- The relationship between Mg deficiency, inflammation, and vitamin A status requires further investigation.
Purpose of the Study:
- To investigate the impact of the acute phase response in magnesium-deficient rats on vitamin A status.
- To determine if Mg deficiency influences plasma retinol and retinol-binding protein (RBP) levels.
- To assess the effect of Mg deficiency on liver retinol reserves.
Main Methods:
- Induction of experimental magnesium deficiency in a rat model.
- Observation of clinical symptoms indicative of an acute phase response.
- Measurement of plasma retinol and plasma retinol-binding protein (RBP) concentrations.
- Analysis of liver retinol reserves.
Main Results:
- Mg-deficient rats exhibited clinical signs of an acute phase response.
- A significant reduction in plasma retinol and RBP was observed in Mg-deficient rats.
- Hyporetinemia occurred without a corresponding decrease in hepatic retinol levels.
- The findings suggest a link between Mg deficiency-induced inflammation and decreased RBP.
Conclusions:
- Mg deficiency in rats leads to hyporetinemia primarily through a reduction in RBP, not depletion of liver vitamin A.
- The inflammatory effects associated with Mg deficiency appear to impact vitamin A transport and status.
- Plasma retinol levels may not be a reliable indicator of vitamin A status in conditions of Mg deficiency and inflammation.
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