Diet-induced obese rats have higher iron requirements and are more vulnerable to iron deficiency

Purpose

Since obesity is associated with poorer iron status, the effects of diet-induced obesity on iron status and iron-regulatory pathways were examined.

Methods

Weanling male diet-induced obese sensitive (n = 12/diet group) and resistant (n = 12/diet group) rats were fed one of four high-fat, high-energy diets supplemented with 5 (5Fe, low), 15 (15Fe, marginal), 35 (35Fe, normal) or 70 (70Fe, high) mg iron/kg diet for 12 weeks. At the end of the study, rats in each diet group were categorised as obese (>19 %) or lean (<17 %) based on percentage body fat.

Results

Obese rats gained more weight, had larger total lean mass, consumed more food and showed greater feed efficiency compared with lean rats. Obese rats fed the 5Fe and 15Fe diets had poorer iron status than lean rats fed the same diet. Obese 5Fe rats had lower serum iron and more severe iron-deficiency anaemia. Obese 15Fe rats had lower mean corpuscular haemoglobin and liver iron concentrations. Hepcidin mRNA expression in liver and adipose tissue was similar for obese and lean rats. Iron concentration and content of the iron transporters divalent metal transporter 1 and ferroportin 1 in duodenal mucosa were also similar.

Conclusions

Obese rats that were larger, regardless of adiposity, had higher iron requirements compared with lean rats that appeared independent of hepcidin, inflammation and intestinal iron absorption. Higher iron requirements may have resulted from larger accretion of body mass and blood volume. Greater food consumption did not compensate for the higher iron needs, indicating increased susceptibility to iron deficiency.     

Goat milk supplemented with folic acid protects cell biomolecules from oxidative stress-mediated damage after anaemia recovery in comparison with cow milk

Background

Fe overload is a common consequence of the anaemia treatment, increasing the oxidative stress and promoting the accumulation of damaged biomolecules, with the subsequently impairment of cell functions. Oxidative stress and the role of folic acid preventing free radical damage have been extensively studied; nevertheless, no studies are available about the influence of folic acid-supplemented goat milk consumption on the oxidative stress-mediated damage.

Aim

The objective of the present study was to assess the influence of folic acid supplementation of goat milk- or cow milk-based diets, after Fe-overload treatment to palliate anaemia, on oxidative stress-mediated biomolecular damage in the liver, brain, erythrocytes, duodenal mucosa and plasma.

Methods

Control and anaemic rats were fed goat milk- or cow milk-based diets, either with normal Fe or Fe overload (450 mg/kg), and normal folic acid (2 mg/kg) or folic acid supplemented (40 mg/kg) for 30 days.

Results

During chronic Fe repletion, background DNA damage was significantly lower in anaemic rats fed folic acid-supplemented goat milk-based diet, as revealed by tail DNA (%), and folic acid-supplemented goat milk also had a beneficial effect, reducing the extent of lipid peroxidation in liver, plasma, erythrocytes and especially in brain and duodenal mucosa. Furthermore, protein oxidative damage was lower in anaemic rat duodenal mucosa for all goat milk-based diets.

Conclusions

Folic acid supplement in goat milk avoids the undesirable effects of Fe overload during anaemia recovery in all the tissues studied, especially in the liver and duodenal mucosa, which are the tissues with higher exposition to dietary Fe.     

Effect of carnitine,acetyl-, and propionylcarnitine supplementation on the body carnitine pool,skeletal muscle composition,and physical performance in mice

Purpose

Pharmacokinetics and effects on skeletal muscle and physical performance of oral acetylcarnitine and propionylcarnitine are not well characterized. We therefore investigated the influence of oral acetylcarnitine, propionylcarnitine, and carnitine on body carnitine homeostasis, energy metabolism, and physical performance in mice and compared the findings to non-supplemented control animals.

Methods

Mice were supplemented orally with 2 mmol/kg/day carnitine, acetylcarnitine, or propionylcarnitine for 4 weeks and studied either at rest or after exhaustive exercise.

Results

In the supplemented groups, total plasma and urine carnitine concentrations were significantly higher than in the control group receiving no carnitine, whereas the skeletal muscle carnitine content remained unchanged. The supplemented acylcarnitines were hydrolyzed in intestine and liver and reached the systemic circulation as carnitine. Bioavailability of carnitine and acylcarnitines, determined as the urinary excretion of total carnitine, was in the range of 19 %. Skeletal muscle morphology, including fiber-type composition, was not affected, and oxygen consumption by soleus or gastrocnemius fibers was not different between the groups. Supplementation with carnitine or acylcarnitines had no significant impact on the running capacity, but was associated with lower plasma lactate levels and a higher glycogen content in white skeletal muscle after exhaustive exercise.

Conclusions

Oral supplementation of carnitine, acetylcarnitine, or propionylcarnitine in mice is associated with increased plasma and urine total carnitine concentrations, but does not affect the skeletal muscle carnitine content. Despite better preservation of skeletal muscle glycogen and lower plasma lactate levels, physical performance was not improved by carnitine or acylcarnitine supplementation.     

Exercise training and supplementation with carnitine and antioxidants increases carnitine stores, triglyceride utilization, and endurance in exercising rats

This study evaluated the effects of supplementation of carnitine and antioxidants on lipids, carnitine concentrations, and exercise endurance time in both trained and untrained rats as compared to non-supplemented rats. Thirty-two male SD rats, age 7 wk were divided into four groups according to exercise training and modified AIN-76 diets: NTNS (non-trained non-supplemented), NTS (non-trained supplemented), LTNS (long-trained non-supplemented) and LTS (long-trained supplemented). The trained rats were run on a treadmill for 60 min per day (10(0) incline, 20 m/min for 8 wk). Carnitine (0.5%/diet) and vitamin E (0.5 mg/g b.w.) were supplemented in rat diets and vitamin C (0.5 mg/g b.w.) and melatonin (1 microg/g b.w.) were administered into the stomachs of the rats. LTNS and LTS rats had significantly lower serum total lipid, triglyceride, total cholesterol and liver triglycerides, but had higher serum HDL-cholesterol. There were no changes in exercise endurance time by supplementation in untrained animals, however endurance times were longer in LTS animals than in LTNS. The supplementation and training tended to increase carnitine palmitoyltransferase (CPT-I) activities, although the differences were not statistically significant. Likewise, CPT-I mRNA levels were higher in both supplemented and exercise trained rats. These results suggest that supplementation of carnitine and antioxidants may improve lipid profiles and exercise ability in exercise-trained rats.     

Anti-anaemia efficacy of β-lactoglobulin hydrolysate-iron complex on iron-deficient anaemic rats

Purpose

The effects of orally administered β-lactoglobulin hydrolysate-iron complex (β-LGH-Fe) on haematological and biochemical parameters in anaemic rats were evaluated. Female weaning Sprague–Dawley rats were fed with iron-deficient diet to induce iron deficiency anaemia. After 6 weeks, the obtained anaemic rats were divided into five groups: iron deficiency control group (iron-deficient diet without β-LGH-Fe complex supplementation, IDC); three groups supplemented with different dosages of β-LGH-Fe complex (0.5 mg Fe/kg BW, iron-deficient diet with low β-LGH-Fe, IDLFe; 2.0 mg Fe/kg BW, iron-deficient diet with medium β-LGH-Fe, IDMF; 4.0 mg Fe/kg BW, iron-deficient diet with high β-LGH-Fe, IDHFe); and ferrous sulphate-supplemented group at a dosage of 2.0 mg Fe/kg BW.

Results

β-LGH-Fe complex could significantly improve hematocrit and haemoglobin decrease, and normalise the serum iron level, total iron-binding capacity and transferrin saturation of anaemic rats in a dose-dependent manner. Serum ferritin content and hepatic nonheme iron level were also increased. In addition, the antioxidant enzyme activities of superoxidase dismutase, catalase and glutathione peroxidase in both plasma and liver homogenate were improved. The production of malondialdehyde and pro-inflammatory cytokines (TNF-α and IL-6) decreased.

Conclusions

It suggests that β-LGH-Fe complex can ameliorate iron deficiency anaemia, which might make it a potential ingredient with anti-anaemia activity.     

Both iron deficiency and daily iron supplements increase lipid peroxidation in rats

Numerous studies have shown that iron-loaded diets increase markers of lipid peroxidation in rats, but few have addressed the effects of oral iron supplements on these markers. We investigated the effects of daily and intermittent iron supplements on iron and vitamin E status, and lipid peroxidation. Iron supplements were administered in doses equivalent to those often given to pregnant women in the developing world. In Study 1, iron-deficient (D) and iron-normal (N) rats were fed either 0 or 8000 microgram of supplemental iron daily for 21 d. In Study 2, D rats were fed either the same supplements daily or once every 3 d (8 supplements total). Lipid peroxidation was assessed by breath ethane and pentane and by malondialdehyde (MDA) (using GC-MS). In Study 1, daily supplemented N and D rats had liver nonheme iron concentrations that were 1.8- and 2.7-fold higher, respectively, than those in unsupplemented N rats. Breath ethane levels were also higher in supplemented rats (P < 0.05), but MDA (in plasma, liver, kidney) and liver vitamin E did not differ. Unexpectedly, severely D, anemic rats had significant elevations in the levels of breath ethane, liver MDA and kidney MDA. In Study 2, liver iron and breath ethane decreased progressively (P < 0.05) from 1 d to 3 d after the last iron dose in intermittently supplemented rats. We conclude that iron deficiency results in lipid peroxidation, but that its correction with daily iron supplements results in abnormal iron accumulation and increased lipid peroxidation in rats. These effects are mitigated by intermittent iron supplementation.     

Four-week ingestion of blood orange juice results in measurable anthocyanin urinary levels but does not affect cellular markers related to cardiovascular risk: a randomized cross-over study in healthy volunteers

Purpose

Blood orange juice (OJ) is an important source of anthocyanins (ACN). The latter molecules are endowed with antioxidant activity and might thus modulate different cell function. Our aim was to investigate ACN absorption following a 1-month daily supplementation of blood OJ and their potential effects on cell markers of platelet and leukocyte activation and interaction.

Methods

Eighteen healthy subjects (10 men and 8 women) were supplemented for 4?weeks with 1?L/day of either blood OJ or blond OJ (that contains no ACN), following a cross-over design. Blood samples were obtained from fasting participants both at baseline and after each week of treatment to measure plasma ACN concentration. At the same time-intervals, 24-h urinary excretion of these molecules was also measured. At the beginning and the end of each 4-week intervention period, platelet and leukocyte markers and mixed cell conjugates were assessed both in basal condition and upon in vitro collagen/ADP activation.

Results

After 1?week supplementation with blood OJ, 24-h urinary excretion of ACN reached average levels of 11.47?±?5.63?nmol that significantly differed from baseline and remained substantially unchanged until the end of treatment. No plasma accumulation of ACN following blood OJ supplementation was observed. Cellular markers were not significantly affected by either OJ after 4-week supplementation.

Conclusions

Following supplementation of healthy volunteers with 1 L/day of blood OJ for 4?weeks, the ACN plasma levels reached were insufficient to significantly modify cell markers of platelet and leukocyte activation and interaction.     

Redistribution of vitamin A after iron supplementation in Indonesian infants

BACKGROUND: Deficiencies of iron and vitamin A are prevalent worldwide. Single-micronutrient supplementation is widely used to combat these deficiencies. However, micronutrient deficiencies often occur concurrently, and there are many interactions between micronutrients. OBJECTIVE: This study investigated interactions among 3 important micronutrients--iron, vitamin A, and zinc--when they are given as supplements. DESIGN: In a randomized, double-blind, placebo-controlled supplementation trial, 387 Indonesian infants aged 4 mo were supplemented 5 d/wk for 6 mo with 10 mg Fe, 10 mg Zn, 2.4 mg beta-carotene, 10 mg each of Fe and Zn, 10 mg Zn + 2.4 mg beta-carotene, or placebo. Complete data on micronutrient status, including hemoglobin, ferritin, retinol, zinc, and the modified relative dose response (a measure of liver retinol stores), were available from 256 infants at the end of the study. RESULTS: Iron-supplemented infants had significantly lower plasma retinol concentrations and a significantly higher prevalence of vitamin A deficiency, as defined by a plasma retinol concentration <0.70 micromol/L, than did the non-supplemented infants. In contrast, the modified relative dose response of the iron-supplemented infants indicated greater liver stores of vitamin A. Iron supplementation improved iron status, and zinc supplementation improved zinc status, but beta-carotene supplementation did not significantly improve vitamin A status. CONCLUSIONS: In this study, iron supplementation in infants with marginal vitamin A status led to lower plasma vitamin A concentrations and simultaneously to greater vitamin A liver stores. This implies a redistribution of retinol after iron supplementation, which might induce vitamin A deficiency. Therefore, iron supplementation in infants should be accompanied by measures to improve vitamin A status.     

Predictors of haemoconcentration at delivery: association with low birth weight

Propose

To assess the factors associated with risk of haemoconcentration at delivery, such as initial haemoglobin levels and alterations in the HFE gene, and its effect on low birth weight in pregnant women supplemented with moderate doses of iron.

Methods

Case–control study nested in a longitudinal study conducted on 217 healthy pregnant women taking moderate iron supplementation and their newborns. Women were classified according to the risk of haemoconcentration at delivery, defined as Hb > 130 g/L. Each subject’s obstetric and clinical history, smoking habit, and iron biochemical parameters (haemoglobin (Hb), serum ferritin and transferrin saturation) were recorded at 1st, 2nd and 3rd trimester and at delivery. Polymorphisms of the HFE gene (C282Y, H63D and S65C) were also measured.

Results

The average of iron supplementation of all the women was 43.9 mg/dia (geometric mean, 95 % CI: 43.6–44.1). Higher levels of Hb at early gestation and the presence of HFE mutations were associated with greater risk of haemoconcentration at delivery, adjusted odds ratios of 1.14 (95 % CI: 1.05–1.25) and 5.35 (95 % CI: 1.6–17.8). Haemoconcentration at delivery was associated with a greater risk of low birth weight, adjusted odd ratio of 11.48 (95 % CI: 1.13–116.6).

Conclusions

Moderate daily doses of supplementary iron may be harmful for foetal growth in women with alterations in HFE gene and who started pregnancy with good haemoglobin levels. Overall, this suggests the importance of determining a woman’s iron status early in her pregnancy in order to establish a more appropriate pattern of supplementation.     

The effect of methionine supplementation of the AIN-93G semi-synthetic diet on the levels of homocysteine and lipids in experimental rats

Objectives

The studies were carried out on 36 growing albino Wistar rats.

Participants/Measurements

The animals were randomly divided into six equinumerous groups (six rats per group), and were fed six different diets for 42 days. The control group (I) was fed with AIN-93G semi-synthetic diet, whereas groups II–VI were fed with AIN-93G semi-synthetic diet supplemented with: 2, 4, 8, 16 and 32 g of methionine/kg diet, respectively. There were assessed enzymatically, in rats’ blood serum, the contents of homocysteine, total cholesterol, HDL fraction and triacyloglicerols. In addition, the LDL+VLDL cholesterol content was calculated.

Results

The methionine content of the diet was found to be highly positively correlated with the homocysteine content (r = 0.981) and negatively correlated with the triacylglycerols content (r = ?0.916) of the experimental animals’ blood serum.

Conclusion

In the blood serum of rats fed the highest-methionine diet (32 g methionine/kg diet), the homocysteine content was significantly higher, as were the levels of total cholesterol and its HDL fraction, while the triacylglycerols content was lower as compared to the values obtained for rats fed other diet types.     

Ellagic acid attenuates high-carbohydrate, high-fat diet-induced metabolic syndrome in rats

Background

Fruits and nuts may prevent or reverse common human health conditions such as obesity, diabetes and hypertension; together, these conditions are referred to as metabolic syndrome, an increasing problem. This study has investigated the responses to ellagic acid, present in many fruits and nuts, in a diet-induced rat model of metabolic syndrome.

Methods

Eight- to nine-week-old male Wistar rats were divided into four groups for 16-week feeding with cornstarch diet (C), cornstarch diet supplemented with ellagic acid (CE), high-carbohydrate, high-fat diet (H) and high-carbohydrate, high-fat diet supplemented with ellagic acid (HE). CE and HE rats were given 0.8 g/kg ellagic acid in food from week 8 to 16 only. At the end of 16 weeks, cardiovascular, hepatic and metabolic parameters along with protein levels of Nrf2, NF-κB and CPT1 in the heart and the liver were characterised.

Results

High-carbohydrate, high-fat diet-fed rats developed cardiovascular remodelling, impaired ventricular function, impaired glucose tolerance, non-alcoholic fatty liver disease with increased protein levels of NF-κB and decreased protein levels of Nrf2 and CPT1 in the heart and the liver. Ellagic acid attenuated these diet-induced symptoms of metabolic syndrome with normalisation of protein levels of Nrf2, NF-κB and CPT1.

Conclusions

Ellagic acid derived from nuts and fruits such as raspberries and pomegranates may provide a useful dietary supplement to decrease the characteristic changes in metabolism and in cardiac and hepatic structure and function induced by a high-carbohydrate, high-fat diet by suppressing oxidative stress and inflammation.     

Effects of margarine supplemented with T10C12 and C9T11 CLA on atherosclerosis and steatosis in apoE/LDLR -/- mice

Objectives

The objective of this study was to evaluate functional effects of margarine supplemented with individual CLA isomers trans-10, cis-12 and cis-9, trans-11 in apoE/LDLR -/- mice.

Design

In LONG experiment (LONG), two-month old mice with no atherosclerosis were assigned to experimental groups and fed for the next 4 months. In SHORT experiment (SHORT), four-month old mice, with pre-established atherosclerosis, were assigned to experimental groups and fed for the next 2 months. The experimental diets were: ALN-93G (margarine), AIN-93G + 0.5% trans-10, cis-12 CLA (tl0cl2), and AIN-93G + 0.5% cis-9, trans-11 CLA (c9tll).

Results

In both experiments (LONG and SHORT), liver weight was significantly (P<0.05) increased in mice fed t110c12 CLA. Hepatic steatosis was found in animals fed t110c12 diet and no signs of the steatosis was observed in mice fed c9tll CLA. Dietary treatments with t110c12 CLA significantly increased total plasma cholesterol and plasma triacylglycerols. There were no isomer-specific effects of CLA isomers on area of atherosclerotic plaque in aortic root.

Conclusion

In conclusion, t110c12 CLA significantly increased liver weight in mice in LONG and SHORT experiments. Our results do not support the notion that CLA isomer supplementation to the margarine possess anti-atheroclerotic effect. Therefore, no isomer-specific effects of CLA on development of atherosclerosis were observed.     

Micronutrient status in lactating mothers before and after introduction of fortified flour: cross-sectional surveys in Maela refugee camp

Background

Deficiency of micronutrients is common in refugee populations.

Objectives

Identify deficiencies and whether provided supplements and wheat flour fortified with 10 micronutrients impacts upon status among breast-feeding women from Maela refugee camp.

Methods

Two sequential cross-sectional studies were conducted in different groups of lactating mothers at 12?weeks postpartum. The first survey was before and the second 4–5?months after micronutrient fortified flour (MFF) had been provided to the camp (in addition to the regular food basket). Iron status and micronutrients were measured in serum, whole blood, and in breast milk samples.

Results

Iron and zinc deficiency and anemia were highly prevalent while low serum retinol and thiamine deficiency were rarely detected. Iron and zinc deficiency were associated with anemia, and their proportions were significantly lower after the introduction of MFF (21 vs. 35% with soluble transferrin receptor (sTfR) >8.5?mg/L, P?=?0.042, and 50 vs. 73% with serum zinc <0.66?mg/L, P?=?0.001). Serum sTfR, whole-blood thiamine diphosphate (TDP) and serum β-carotene were significant predictors (P?Conclusions High whole-blood TDP and breast milk thiamine reflected good compliance to provided thiamine; high prevalence of iron deficiency suggested insufficient dietary iron and low acceptance to ferrous sulfate supplements. MFF as an additional food ration in Maela refugee camp seemed to have an effect in reducing both iron and zinc deficiency postpartum.     

Effects of excessive dietary methionine on oxidative stress and dyslipidemia in chronic ethanol-treated rats

BACKGROUND/OBJECTIVE

The aim of this study was to examine the effect of high dietary methionine (Met) consumption on plasma and hepatic oxidative stress and dyslipidemia in chronic ethanol fed rats.

MATERIALS/METHODS

Male Wistar rats were fed control or ethanol-containing liquid diets supplemented without (E group) or with DL-Met at 0.6% (EM1 group) or 0.8% (EM2 group) for five weeks. Plasma aminothiols, lipids, malondialdehyde (MDA), alanine aminotransferase (ALT), and aspartate aminotransferase were measured. Hepatic folate, S-adenosylmethionine (SAM), and S-adenosylhomocysteine (SAH) were measured.

RESULTS

DL-Met supplementation was found to increase plasma levels of homocysteine (Hcy), triglyceride (TG), total cholesterol (TC), and MDA compared to rats fed ethanol alone and decrease plasma ALT. However, DL-Met supplementation did not significantly change plasma levels of HDL-cholesterol, cysteine, cysteinylglycine, and glutathione. In addition, DL-Met supplementation increased hepatic levels of folate, SAM, SAH, and SAM:SAH ratio. Our data showed that DL-Met supplementation can increase plasma oxidative stress and atherogenic effects by elevating plasma Hcy, TG, and TC in ethanol-fed rats.

CONCLUSION

The present results demonstrate that Met supplementation increases plasma oxidative stress and atherogenic effects by inducing dyslipidemia and hyperhomocysteinemia in ethanol-fed rats.     

Vitamin D supplementation,bone turnover,and inflammation in HIV-infected patients

Objective

To assess whether vitamin D supplementation could be associated with a modification of inflammatory markers and bone turnover in HIV-1-infected patients.

Effect of dairy fat on plasma phytanic acid in healthy volunteers - a randomized controlled study

Background and Aims

The effect of red palm oil (RPO) supplementation on infarct size after ischaemia/reperfusion in a cholesterol enriched diet-induced hyperlipidemic animal model has not been reported. Previous studies reported results on the effect of RPO in a normal diet, whilst evidence of protection has been linked to improved functional recovery, prosurvival kinase, anti-apoptosis and NO-cGMP. Therefore, we aimed to investigate the effects of dietary RPO supplementation in a cholesterol-enriched diet-induced hyperlipidemic rat model and to investigate the involvement of matrix metalloproteinase 2 (MMP2) inhibition as a possible mechanism of protection.

Materials and Methods

Male Wistar rats were fed either a standard rat chow diet (Norm) or a 2% cholesterol-enriched diet (Chol) for nine weeks. Additionally, two more groups received the same treatment, however, at the week 4, diet was supplemented with RPO for the last five weeks (Norm+RPO and Chol+RPO), respectively. After the feeding period hearts were isolated, perfused according to Langendorff and subjected to 30 minutes of normothermic global ischaemia followed by two hours of reperfusion. Infarct size was measured by 2,3,5-triphenyltetrazolium chloride staining at the end of reperfusion.

Results

Cholesterol-enriched diet increased myocardial infarct size from 23.5 ± 3.0% to 37.2 ± 3.6% (p < 0.05) when compared to normal diet. RPO supplementation significantly reduced infarct size either in Norm+RPO or in Chol+RPO (to 9.2 ± 1.0% and 26.9 ± 3.0%), respectively. Infarct size in Chol+RPO was comparable to the Norm group. MMP2 activity before ischaemia was significantly reduced in the Chol+RPO group when compared to the Chol group. However, the MMP2 activity of the hearts of the RPO fed rats was significantly increased when compared to the normal diet group after ischaemia.

Conclusions

For the first time it was shown that dietary RPO supplementation attenuated the increased susceptibility of the hearts in cholesterol fed rats to ischaemia/reperfusion injury. This was shown by reduced infarct size. For the first time we also show that red palm oil supplementation altered pre-ischaemic levels of MMP-2, which may indicate that myocardial MMP2 may be implicated as a possible role player in RPO mediated protection against ischaemia/reperfusion injury in hearts of cholesterol supplemented rats.     

Bone mineral density and content during weight cycling in female rats: effects of dietary amylase-resistant starch

Background

Although there is considerable evidence for a loss of bone mass with weight loss, the few human studies on the relationship between weight cycling and bone mass or density have differing results. Further, very few studies assessed the role of dietary composition on bone mass during weight cycling. The primary objective of this study was to determine if a diet high in amylase-resistant starch (RS₂), which has been shown to increase absorption and balance of dietary minerals, can prevent or reduce loss of bone mass during weight cycling.

Methods

Female Sprague-Dawley (SD) rats (n = 84, age = 20 weeks) were randomly assigned to one of 6 treatment groups with 14 rats per group using a 2 × 3 experimental design with 2 diets and 3 weight cycling protocols. Rats were fed calcium-deficient diets without RS₂ (controls) or diets high in RS₂ (18% by weight) throughout the 21-week study. The weight cycling protocols were weight maintenance/gain with no weight cycling, 1 round of weight cycling, or 2 rounds of weight cycling. After the rats were euthanized bone mineral density (BMD) and bone mineral content (BMC) of femur were measured by dual energy X-ray absorptiometry, and concentrations of calcium, copper, iron, magnesium, manganese, and zinc in femur and lumbar vertebrae were determined by atomic absorption spectrophotometry.

Results

Rats undergoing weight cycling had lower femur BMC (p < 0.05) and marginally lower BMD (p = 0.09) than rats not undergoing weight cycling. In comparison to controls, rats fed RS₂ had higher femur BMD (p < 0.01) and BMC (p < 0.05), as well as higher values for BMD and BMC measured at the distal end (p < 0.001 and p < 0.01) and femoral neck (p < 0.01 and p < 0.05). Consistent with these findings, RS₂-fed rats also had higher femur calcium (p < 0.05) and magnesium (p < 0.0001) concentrations. They also had higher lumbar vertebrae calcium (p < 0.05) and magnesium (p < 0.05) concentrations.

Conclusion

Weight cycling reduces bone mass. A diet high in RS₂ can minimize loss of bone mass during weight cycling and may increase bone mass in the absence of weight cycling.     

Iron deficiency and anemia in iron-fortified formula and human milk-fed preterm infants until 6 months post-term

Purpose

An iron intake of >2 mg/kg/d is recommended for preterm infants. We hypothesized that human milk (HM)-fed preterm infants require iron supplementation after discharge, whereas iron-fortified formulae (IFF; 0.8–1.0 mg iron/100 ml) may provide sufficient dietary iron until 6 months post-term.

Methods

At term age, 3 and 6 months post-term, ferritin (μg/l) was measured in 92 IFF-fed infants (gestational age (median (interquartile range)) 30.7 (1.4) weeks, birth weight 1,375 (338) gram) and 46 HM-fed infants (gestational age 30.0 (1.7) weeks, birth weight 1,400 (571) gram). Iron intake (mg/kg/d) between term age and 6 months post-term was calculated.

Results

Iron was supplemented to 71.7 % of HM-fed and 83.7 % of IFF-fed infants between term age and 3 months post-term and to 13 % of HM-fed and 0 % of IFF-fed infants between 3 and 6 months post-term. IFF-fed infants had an iron intake from supplements and formula of 2.66 (1.22) mg/kg/d between term age and 3 months post-term and 1.19 (0.32) mg/kg/d between 3 and 6 months post-term. At 3 and 6 months post-term, the incidence of ferritin <12 μg/l was higher in HM-fed compared to IFF-fed infants (23.8 vs. 7.8 % and 26.3 vs. 9.5 %, P < 0.02).

Conclusion

This observational study demonstrates that ferritin <12 μg/l is more prevalent in HM-fed infants until 6 months post-term. This may be due to early cessation of additional iron supplementation. We speculate that additional iron supplementation is not necessary in preterm infants fed IFF (0.8–1.0 mg iron/100 ml), as they achieve ferritin ≥12 μg/l without additional iron supplements between 3 and 6 months post-term.     

Combined dietary folate, vitamin B-12, and vitamin B-6 intake influences plasma docosahexaenoic acid concentration in rats

Background

Folate, vitamin B-12, and vitamin B-6 are essential nutritional components in one-carbon metabolism and are required for methylation capacity. The availability of these vitamins may therefore modify methylation of phosphatidylethanolamine (PE) to phosphatidylcholine (PC) by PE-N-methyltransferase (PEMT) in the liver. It has been suggested that PC synthesis by PEMT plays an important role in the transport of polyunsaturated fatty acids (PUFAs) like docosahexaenoic acid (DHA) from the liver to plasma and possibly other tissues. We hypothesized that if B-vitamin supplementation enhances PEMT activity, then supplementation could also increase the concentration of plasma levels of PUFAs such as DHA. To test this hypothesis, we determined the effect of varying the combined dietary intake of these three B-vitamins on plasma DHA concentration in rats.

Methods

In a first experiment, plasma DHA and plasma homocysteine concentrations were measured in rats that had consumed a B-vitamin-poor diet for 4?weeks after which they were either continued on the B-vitamin-poor diet or switched to a B-vitamin-enriched diet for another 4?weeks. In a second experiment, plasma DHA and plasma homocysteine concentrations were measured in rats after feeding them one of four diets with varying levels of B-vitamins for 4?weeks. The diets provided 0% (poor), 100% (normal), 400% (enriched), and 1600% (high) of the laboratory rodent requirements for each of the three B-vitamins.

Results

Plasma DHA concentration was higher in rats fed the B-vitamin-enriched diet than in rats that were continued on the B-vitamin-poor diet (P?=?0.005; experiment A). Varying dietary B-vitamin intake from deficient to supra-physiologic resulted in a non-linear dose-dependent trend for increasing plasma DHA (P?=?0.027; experiment B). Plasma DHA was lowest in rats consuming the B-vitamin-poor diet (P?>?0.05 vs. normal, P?. enriched and high) and highest in rats consuming the B-vitamin-high diet (P?. poor and normal, P?>?0.05 vs. enriched). B-vitamin deficiency significantly increased plasma total homocysteine but increasing intake above normal did not significantly reduce it. Nevertheless, in both experiments plasma DHA was inversely correlated with plasma total homocysteine.

Conclusion

These data demonstrate that dietary folate, vitamin B-12, and vitamin B-6 intake can influence plasma concentration of DHA.