Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: March 12, 2008
Publication Date: March 12, 2008
Citation: Nielsen, F.H. 2008. Response of rats to 50% of the estimated dietary magnesium requirement changes with length of deprivation and different dietary fat sources. Gordon Research Conferences, Ventura, CA, March 9-14, 2008. Technical Abstract: Magnesium deprivation increased the inflammatory neuropeptide substance P and the inflammatory cytokines TNFa and IL-1ß in bone of rats; the effects of deprivation were more marked at 6 months than 3 months in rats fed 50% of the magnesium requirement (Rude et al., Ostoporosos Int. 17:1022, 2006). Dietary n-3 long chain polyunsaturated fatty acids (LCPUFA) have been shown to decrease indicators of inflammatory stress including plasma C-reactive protein (CRP). Thus, an experiment was performed to determine whether dietary fatty acid composition affects variables associated with the inflammatory response and bone metabolism in rats fed 50% of the estimated magnesium requirement. Weanling female rats were fed diets containing 250 mg (10.3 mmol) magnesium/kg in a factorial arrangement with dietary variables of supplemental magnesium at 0 and 250 mg/kg and fat sources of 75 g/kg safflower oil (mostly n-6 PUFAs) or 65 g/kg fish (menhaden) oil (high in n-3 LCPUFAs) plus 10 g/kg linoleic acid. After 8 and 12 weeks on their respective diets, each rat was placed in a metabolic cage for a 16-hour collection of urine. After 13 weeks, the rats were anesthetized with ether for the collection of blood and tissues. Magnesium deprivation at 13 weeks was confirmed by decreased femur and tibia magnesium concentrations. Magnesium deprivation and fish oil compared to safflower oil also decreased urinary magnesium excretion at both 8 and 12 weeks. The response to magnesium deprivation apparently was changing between 8 and 12 weeks because magnesium deprivation decreased urinary calcium and prostaglandin E2 concentrations (creatinine basis) at 8 weeks but not at 12 weeks. Fish oil compared to safflower oil decreased plasma CRP, which was unaffected by magnesium deprivation. Neither dietary oil nor magnesium significantly affected plasma substance P concentration. Although magnesium deprivation did not affect the inflammatory response indicators, the deprivation apparently affected oxidative stress with some effects depending upon dietary fatty acid composition. Magnesium deprivation increased plasma extracellular superoxide dismutase in rats fed corn oil but not in rats fed fish oil. Magnesium deprivation regardless of dietary oil increased plasma homocysteine, which may increase oxidative stress. Dietary fatty acids also affected the changes in calcium and phosphorus concentrations in various tissues induced by magnesium deprivation. Magnesium deprivation increased the phosphorus concentration in kidneys of rats fed fish oil, but not in rats fed corn oil. In contrast, magnesium deprivation increased heart phosphorus concentration with the effect most marked in rats fed corn oil. Corn oil instead of fish oil decreased tibia phosphorus concentration in magnesium-deprived but not magnesium-adequate rats. Magnesium deprivation increased tibia calcium concentration. In contrast, magnesium deprivation tended to decrease femur calcium concentration in rats fed corn oil but not in rats fed fish oil. The findings suggest that dietary fatty acids, which affect oxidative stress and the inflammatory response, influence the response or rats to a moderate magnesium deprivation, and that this response changes with the length of deprivation.