The Effects of Magnesium Deficiency on Molybdenum Metabolism in Rats
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The Effects of Magnesium Deficiency on Molybdenum Metabolism in Rats Ki Hyun Kim & Masayuki Funaba & Munehiro Yoshida & Tohru Matsui
Received: 24 September 2012 / Accepted: 25 October 2012 / Published online: 8 November 2012 # Springer Science+Business Media New York 2012
Abstract Our previous report indicated that magnesium (Mg) deficiency increased molybdenum (Mo) concentration in the rat liver, suggesting the possibility that Mg deficiency affects Mo metabolism. Growing male rats were given a control diet or a Mg-deficient diet for 4 weeks. Urine and feces were collected during the second and fourth weeks of the feeding trial. The liver, kidney, spleen, skeletal muscle, and blood were collected at the end of the feeding trial. Mg deficiency did not affect the apparent absorption of Mo, but it reduced urinary excretion of Mo. The retention of Mo tended to be higher in the Mg-deficient group than in the control group. Hepatic Mo concentration was higher in the Mg-deficient group than in the control group, but Mg deficiency did not affect Mo concentration in other tissues and plasma. Mg deficiency downregulated the mRNA expression of Mo transporter 2 (MOT2) in the liver, but not in the kidney. These results suggest that Mg deficiency decreases urinary Mo excretion, which is too slight to affect plasma Mo concentration, and that Mg deficiency selectively disturbs the homeostatic mechanism of Mo in the liver, which is not related to the mRNA expression of MOT2 in the liver. Keywords Magnesium deficiency . Molybdenum absorption . Molybdenum excretion . Molybdenum transporter . Liver
K. H. Kim : M. Funaba : T. Matsui (*) Division of Applied Biosciences, Kyoto University Graduate School of Agriculture, Kyoto 606-8502, Japan e-mail: [email protected] M. Yoshida Faculty of Chemistry, Materials and Bioengineering, Kansai University, Osaka, Japan
Introduction Molybdenum (Mo) is an essential trace element in animals; however, Mo deficiency is rare in animals and humans, and Mo toxicity is more likely than Mo deficiency [1]. Mo toxicity is associated with symptoms such as growth depression, reproductive failure, diarrhea, anemia, and gout-like symptoms in both humans and animals [2–5]. Further, Mo toxicity induces an inflammatory response in the liver [6, 7]. Dietary Mo is efficiently absorbed in animals [8, 9] and humans [10]. The absorbed Mo is primarily excreted through urine; thus, urinary Mo excretion is considered to be the key pathway for maintaining Mo homeostasis [11]. Mo concentration was found to be relatively stable in many tissues, including the liver and kidney of rats, even if dietary Mo concentration was fourfold higher than the nutritional requirement [12]. Another study reported that serum Mo concentration increased due to the dietary addition of Mo at a level threefold higher than the requirement in rats, but Mo concentration in the liver and kidney was not affected by this high level of dietary Mo [13]. Although urinary Mo excretion contributes to whole-body Mo homeostasis, another mechanism most
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