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A sensitive and valid marker to assess magnesium (Mg) status in humans is not available. The kinetically determined exchangeable pool masses have been used for other minerals, such as zinc and selenium, as markers of whole-body mineral status. To evaluate the validity of this relationship for Mg, we measured the exchangeable pools of Mg in rats over a range of magnesium dietary intakes. Rats weighing approximately 170 g were fed a control diet (500 mg Mg/kg), a marginally Mg-deficient diet (200 mg/kg) or a severely Mg-deficient diet (60 mg Mg/kg) for 2 wk. Subsequently, rats were administered an intravenous injection of (25)Mg, and the plasma (25)Mg disappearance curve was followed for the next 7 d. The following two methods were employed to analyze the exchangeable pools of Mg: 1) formal compartmental modeling and 2) a simplified determination of the total mass of the rapidly exchangeable Mg pool (EMgP). The mass of the three exchangeable pools (two extracellular pools and one intracellular pool) determined by compartmental analysis decreased in proportion to dietary Mg intake. EMgP, the combined pools of Mg that exchange with the plasma Mg within 48 h, decreased significantly as dietary Mg was lowered. It was positively correlated with conventional markers of Mg status (total Mg in plasma, erythrocyte and tibia Mg levels). Compartmental analysis assesses Mg exchangeable pools more accurately, but determination of EMgP is simpler and faster. Our findings demonstrate that the exchangeable pools of Mg constitute a good marker of Mg status in rats. [ABSTRACT FROM AUTHOR]

Nondigestible inulin-type fructan intake can stimulate intestinal mineral absorption in both humans and animals. However, this stimulatory effect may depend on experimental conditions such as the duration of the experience, mineral levels in the diet, and the animal's physiological status. The aim of this study was to determine the effect of inulin intake on Zn and Cu absorption in rats at different ages. Male Wistar rats (n = 80) of 4 different ages (2,5, 10, and 20 mo) were randomly assigned to a control group or a group administered 3.75% inulin in their diet for 4 d followed by 7.5% inulin for 26 d. Absorption of Zn67 and Cu65 was determined on d 21 of the experiment by fecal monitoring using Zn67 and Cu65 isotopes. Zn and Cu status was also assessed. Absorption of Zn67 and Cu65 was significantly lower in 11- and 21-mo-old rats than in 3- and 6 mo-old-rats. Moreover, inulin intake significantly increased Zn67 and Cu65 absorption. In conclusion, age and dietary inulin intake can significantly affect intestinal absorption of zinc and copper in rats. Further studies are required to explore this effect over longer periods of inulin intake and to test the effects of inulin in humans.

Recent findings indicate that in addition to its hyperlipemic effect, a high fructose diet has a pro-oxidant effect in rats compared with a starch-based diet. Oligofructose (OFS) has already been shown to decrease plasma lipids in rats. We assessed the impact of fructose on oxidative stress by supplementing a high fructose diet with OFS. Rats were fed either a high fructose diet or a starch-based diet, with or without supplementation of 10 g/100 g oligofructose for 4 wk. Regardless of the type of carbohydrate, OFS in the diet produced an enlargement of the cecum and led to a significant increase in the SCFA cecum pool. Fructose feeding was associated with significantly higher insulin plasma concentrations (+63%) in the control groups, whereas insulin plasma concentrations did not differ in rats fed the fructose diet supplemented with OFS. Plasma leptin concentration was significantly lower (approximately 50%) in the OFS-supplemented fructose group compared with the other three groups. Fructose feeding in rats also significantly increased plasma (P < 0.001) and liver (P < 0.001) triglyceride (TG) concentrations and the addition of OFS prevented the TG accumulation induced by fructose in the liver (P < 0.05) and hyperlipemia (P < 0.05). OFS consumption prevented (P < 0.05) the lower plasma vitamin E/TG ratio in rats fed the fructose diet. Control rats fed the fructose diet had high plasma TBARS values compared with rats fed the starch diet, whereas TBARS values remained unchanged when rats were supplemented with OFS. Control rats fed the fructose diet had higher TBARS urine values and higher heart tissue susceptibility to peroxidation compared with rats fed the starch diet, and this effect was significantly reduced by OFS consumption. Further studies are required to identify the mechanisms underlying the protective effect of OFS against the pro-oxidant effect of fructose. However, the potential nutritional benefits of OFS supplementation in fructose-rich diets are suggested.

Magnesium (Mg) status is currently assessed by various biochemical biomarkers, most of which, however, have some limitations. We developed an in vitro blood load test as a new Mg biomarker using a Mg stable isotope. This test is based on the hypothesis that cellular Mg uptake is increased in Mg deficiency. For this purpose, Wister male rats were fed either Mg-deficient or Mg-adequate diets for 1 mo and blood was sampled and incubated with the (25)Mg isotope (10 mg/L) for 2 h at 37 degrees C. Erythrocytes, lymphocytes and platelets were isolated and (25)Mg concentrations were determined by inductively coupled plasma/mass spectrometry. The feasibility of this approach was then tested on human blood. (25)Mg enrichments in erythrocytes, lymphocytes and platelets from Mg-deficient rats were greater than those from controls. (25)Mg enrichment was low in human erythrocytes (3%) compared with rat erythrocytes (38%), whereas high (25)Mg enrichments were obtained in human lymphocytes and platelets, suggesting that lymphocytes and platelets may be more appropriate cells than erythrocytes for examining Mg status in humans with this approach. More studies are required to validate the utilization of this test as a Mg status biomarker in humans.

Recent findings indicate that a high fructose diet has a prooxidant effect in rats compared with a starch diet. Because honey is rich in fructose, the aim of this study was to assess the effect of substituting honey for refined carbohydrates on lipid metabolism and oxidative stress. Rats were fed for 2 wk purified diets containing 65 g/100 g carbohydrates as wheat starch or a combination of fructose and glucose or a honey-based diet prepared by substituting honey for refined carbohydrates (n = 9/group). The same amount of fructose was provided by the honey and fructose diets. The hypertriglyceridemic effect of fructose was not observed when fructose was provided by honey. Compared with those fed starch, fructose-fed rats had a lower plasma alpha-tocopherol level, higher plasma nitrite and nitrate (NOx) levels and were less protected from lipid peroxidation as indicated by heart homogenate TBARS concentration. Compared with those fed fructose, honey-fed rats had a higher plasma alpha-tocopherol level, a higher alpha-tocopherol/triacylglycerol ratio, lower plasma NOx concentrations and a lower susceptibility of heart to lipid peroxidation. Further studies are required to identify the mechanism underlying the antioxidant effect of honey but the data suggest a potential nutritional benefit of substituting honey for fructose in the diet.

The precise mechanisms of intestinal Mg absorption are still unclear and the possibility of an adaptative rise in the fraction of Mg absorbed as Mg intake is lowered is controversial. Mg deficiency has been studied extensively in rats where it is readily produced by dietary depletion. In this study, we investigated the effect of Mg intake on fractional absorption of Mg acutely and after adaptation to graded Mg intake in rats. For this purpose, male Wistar rats (n = 30) were fed a basal semipurified diet containing 600 mg Mg/kg (MgO) for 7 d. Three groups of 10 rats were then formed and fed the basal semipurified diet with 600, 300 or 150 mg Mg/kg, for 28 d. Apparent and true intestinal absorptions and fecal endogenous excretion of Mg were determined at the beginning and end of the experiment. As expected, plasma Mg levels were lower in the deficient groups than in the control by d 4 and differences were more marked at the end of the experiment. Erythrocyte Mg levels were significantly lower at the end of the experiment in the group fed the diet containing 150 mg Mg/kg. The amounts of Mg absorbed were directly proportional to the dietary Mg intakes in all three experimental groups at both testing periods. This indicated that the apparent and true intestinal absorption percentages of Mg were not different in rats fed the three different levels of dietary Mg. These results also show that fecal endogenous excretion of Mg was nearly directly proportional to the dietary Mg intakes. These results argue in favor of a passive diffusional process for intestinal Mg absorption.

Recent studies suggest that free radicals may be involved in tissue injuries induced by magnesium deficiency. The aim of the present study was to assess the effect of magnesium deficiency on free radical production of skeletal muscle tissue. Male Wistar rats were pair-fed from weaning for 12 d either control or Mg-deficient diets containing 960 or 40 mg magnesium/kg diet, respectively. In the Mg-deficient rats, hypomagnesemia was accompanied by significantly lower magnesium and greater calcium concentrations in skeletal muscle tissue. Electron microscopy of skeletal muscle tissue revealed ultrastructural changes, including swelling mitochondria and disorganization of the sarcoplasmic reticulum network. Using the spin-trapping technique, we showed that significantly more hydroxyl radicals were generated in muscle homogenates of Mg-deficient rats. Moreover, the amount of spin trap adducts was increased in the presence of exogenous iron in both groups. In agreement with these observations, a greater concentration of thiobarbituric acid-reactive substances and a lower concentration of thiol groups were found in skeletal muscle of the Mg-deficient group compared with controls. These results strongly support the hypothesis that free radical-mediated injury could contribute to skeletal muscle lesions resulting from magnesium deficiency.

Male Wistar rats were pair-fed from weaning for 6 wk either a copper-deficient diet or a control diet containing sucrose. Hypercholesterolemia in copper-deficient animals was associated with a significantly greater plasma apolipoprotein B concentration and modifications in the lipid composition of triglyceride-rich lipoproteins containing apolipoprotein B. The proportion of triglycerides was elevated and the proportion of cholesterol was reduced in the VLDL + LDL fractions from copper-deficient rats compared with control animals. When the VLDL + LDL fractions were subjected to in vitro copper-induced oxidation, the lipoprotein fractions from copper-deficient rats were more susceptible to oxidative damage than lipoprotein fractions from control rats as indicated by the rate of diene conjugation. Hydroperoxide and thiobarbituric acid-reactive substance (TBARS) measurements performed 3 h after the induction of peroxidation were in agreement with the greater formation of conjugated dienes. Concentrations of TBARS were significantly greater in heart homogenates from copper-deficient rats compared with control rats. After exposure of tissue homogenates to iron-induced lipid peroxidation, TBARS were significantly higher in liver and heart from copper-deficient rats compared with control rats. Of particular importance is the observation that copper deficiency has a harmful effect on lipid peroxidation in the cardiovascular system.

Weanling rats were pair-fed for 8 d with control and Mg-deficient diets containing 960 and 30 mg of Mg/kg, respectively. The marked reduction in plasma Mg levels indicated that the rats fed the Mg-deficient diet were indeed deficient. In the Mg-deficient rats the percent composition of triglycerides in VLDL, LDL and HDL was elevated and that of protein was reduced. Although the proportion of cholesterol was reduced in LDL and HDL, that of phospholipid was decreased only in HDL. Magnesium deficiency induced a decrease in the percent composition of apolipoprotein (apo) E and a relative increase in the apo C for VLDL. In HDL from Mg-deficient rats, the proportion of apo AI was higher than normal, apo AIV was lower than normal and apo E was virtually absent. The percent composition of oleic and linoleic acids was increased but that of stearic and arachidonic acids was depressed in both VLDL and HDL derived from Mg-deficient rats compared with pair-fed controls. Whether these alterations in lipoprotein profile contribute to hyperlipoproteinemia or are the results of the metabolic changes that produce hyperlipoproteinemia remain to be determined.

This study was conducted to examine the effects of a combination of several dietary fibers (5% guar gum, 5% apple pectin, 15% wheat bran, 22% soybean fiber) and crude potato starch (23%) on plasma lipids and lipoproteins and on liver lipid concentration in rats fed a diet containing either 15% lard or 5% oil with or without dietary cholesterol/cholic acid. Male Wistar rats ate the test diets for 3 wk. The incorporation of fiber and crude potato starch into the diet resulted in a significant enlargement of the cecum; it also increased the concentration of volatile fatty acids and the pool of acetate, propionate and butyrate. Feeding this fermentable carbohydrate decreased plasma cholesterol and triglyceride levels in rats given a low fat diet and prevented the expected rise in plasma cholesterol and triglycerides in rats fed cholesterol/cholic acid or lard. Further studies of high density lipoprotein (HDL) composition, 3-hydroxy-3-methyl-glutaryl coenzyme A reductase (HMG-CoA reductase) activity and 125I-labeled human low density lipoprotein (LDL) turnover were done in the group fed the low fat diet without added cholesterol/cholic acid. The study of the HDL fraction in rats fed a diet rich in fermentable carbohydrates demonstrated a decrease in the HDL1 subpopulation and in the proportion of apolipoprotein E. Plasma clearance of intravenously injected 125I-labeled LDL was faster in rats fed this diet than in rats fed the fiber-free diet. In the liver, cholesterol and triglyceride levels were depressed whereas the activity of HMG-CoA reductase was increased.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of acute magnesium deficiency on lipid metabolism were examined in weaning rats fed a high carbohydrate diet containing starch or sucrose for 8 days. Rats were killed after the feeding period. In plasma, magnesium deficiency increased triglyceride and free cholesterol levels and decreased esterified cholesterol levels. Rats fed a magnesium-deficient diet containing sucrose showed particularly high triglyceride plasma levels. In liver, magnesium-deficient rats fed sucrose showed a significant increase in triglycerides, lactate and alpha-glycerophosphate and a significant decrease in glycogen. Changes in triglycerides and glycogen in the liver of magnesium-deficient rats fed starch were not significant. In sucrose-fed rats, serum lipoproteins were isolated by ultracentrifugation. With magnesium deficiency, triglycerides were significantly increased in the very low density lipoprotein (VLDL) and low density lipoprotein (LDL) fractions and cholesterol levels were increased in the VLDL and LDL and significantly lower in the high density lipoprotein (HDL) fractions. The detrimental effect of severe magnesium deficiency associated particularly with a high carbohydrate diet content and more especially with a sucrose diet is discussed.

Weanling Wistar rats were pair-fed for 8 days control and magnesium-deficient diets. Acute magnesium deficiency increased plasma triglycerides and free cholesterol levels and decreased esterified cholesterol levels. The plasma activity of lecithin--cholesterol acyltransferase was markedly diminished in fasting magnesium-deficient rats (54% reduction) and plasma high density lipoprotein (HDL) free cholesterol was significantly increased in the HDL fraction. The results of this study showing that dietary magnesium affects the activity of the enzyme involved in the esterification of free cholesterol to cholesterol ester provide a possible basis for the reduced plasma cholesterol esterification and hyperlipidemia associated with acute magnesium deficiency.

Weanling Wistar rats were pair-fed for 9 days a control or a calcium-deficient diet. After a 12-hour fast the rats were injected intraperitoneally with glucose (250 mg/100 g body weight), and blood was collected 15, 30 and 60 minutes after the injection. Before injection, calcium (9.7 +/- 0.2 mg/100 ml), glucose and insulin plasma levels were identical in the control and deficient animals, although calcium-deficient animals showed a small but significant increase in blood plasma magnesium levels. Blood glucose levels were higher in the calcium-deficient rats than in control rats 15 to 30 minutes after the glucose injection (15.4 +/- 1.4 vs. 9.7 +/- 0.4 mM, P less than 0.01, 30 minutes after). Plasma insulin levels were significantly lower 15 minutes after the glucose injection (24 +/- 4 vs. 73 +/- 8 microU/ml; P less than 0.01). Calcium deficiency is therefore associated with a decreased response to the glucose tolerance test in the absence of any change in the blood plasma calcium levels.