Antimicrobial Properties of Magnesium Open Opportunities to Develop Healthier Food.

Magnesium is a vital mineral that takes part in hundreds of enzymatic reactions in the human body. In the past several years, new information emerged in regard to the antibacterial effect of magnesium. Here we elaborate on the recent knowledge of its antibacterial effect with emphasis on its ability to impair bacterial adherence and formation complex community of bacterial cells called biofilm. We further talk about its ability to impair biofilm formation in milk that provides opportunity for developing safer and qualitative dairy products. Finally, we describe the pronounced advantages of enrichment of food with magnesium ions, which result in healthier and more efficient food products.

Enrichment of milk with magnesium provides healthier and safer dairy products.

Biofilms on the surfaces of milk-processing equipment are often a major source of contamination of dairy products. Members of the genus Bacillus appear to be among the most commonly found bacteria in dairy farms and processing plants. Bacillus species may thrive in dairy farm equipment and in dairy products since they can form robust biofilms during growth within milk. We found that fortification of milk with magnesium mitigated biofilm formation by Bacillus species, and thus could notably reduce dairy product spoilage. We also show that the mode of action of Mg2+ ions is specific to inhibition of transcription of genes involved in biofilm formation. Our further findings indicate that in the presence of Mg2+ bacterial cells are hypersensitive to the heat pasteurization applied during milk processing. Additionally, we demonstrated that enrichment of milk with magnesium improved technological properties of milk products such as soft cheeses. Finally, we report that there is a notable increase in the intestinal bioavailability potential of magnesium from supplemented milk compared with that from non-supplemented milk.

Human milk fatty acids composition is affected by maternal age.

Human colostrums and transition milk were collected from women under the age of 37 years and women aged 37 years and older. Transition milk of the younger group had lower fat content and 10-fold higher concentrations of omega 6 FA, eicosadecanoic, and arachdonic acids. Gestational age affected the colostrum concentration of total fat and omega 3 and omega 6 FA composition only in the older group. We concluded that age may be a factor in the FA composition of human milk. This should be taken into account when planning diets for pregnant women of different ages.

Vitamin A and the epigenome.

The epigenetic phenomena refer to heritable changes in gene expression other than those in the DNA sequence, such as DNA methylation and histone modifications. Major research progress in the last few years has provided further proof that environmental factors, including diet and nutrition, can influence physiologic and pathologic processes through epigenetic alterations, which in turn influence gene expression. This influence is termed nutritional epigenetics, and one prominent example is the regulation of gene transcription by vitamin A through interaction to its nuclear receptor. Vitamin A is critical throughout life. Together with its derivatives, it regulates diverse processes including reproduction, embryogenesis, vision, growth, cellular differentiation and proliferation, maintenance of epithelial cellular integrity and immune function. Here we review the epigenetic role of vitamin A in cancer, stem cells differentiation, proliferation, and immunity. The data presented here show that retinoic acid is a potent agent capable of inducing alterations in epigenetic modifications that produce various effects on the phenotype. Medical benefits of vitamin A as an epigenetic modulator, especially with respect to its chronic use as nutritional supplement, should rely on our further understanding of its epigenetic effects during health and disease, as well as through different generations.

Fatty acids composition of human milk fed to small for gestational age infants.

OBJECTIVES: To test the null hypothesis that mothers of asymmetric small for gestational age (SGA) infants produce milk with fatty acids composition similar to that of lactating mothers of appropriate-for-gestational-age (AGA) infants. METHODS: We obtained human milk (HM) from 2 groups of lactating volunteers that gave birth to asymmetric SGA (study group) or AGA infants (control group). Each mother was asked to contribute by manual expression at least one of 3 samples: first 72 hours after labor (colostrum), day 2-7 postpartum (transitional milk) and 14 days post partum (mature milk). After lipid extraction using Folch's cold-extraction procedure fatty acids were analyzed using gas chromatography. RESULTS: A total of 108 samples were obtained in 60 women. In univariate analysis, there were no significant differences in any of the fatty acids concentrations examined between groups. This remained true when timing of the sample (colostrum, transitional or mature milk) or gestational age were introduced as confounders in analysis of variance (general linear model). CONCLUSION: Fatty acid composition of human milk is not affected by whether or not the infant was fetal growth restricted. We suggest that mothers of SGA infants may be reassured about the fat quality of their milk.

Vitamin A exerts its antiinflammatory activities in colitis through preservation of mitochondrial activity.

OBJECTIVES: The aim of this study was to assess the protective effects of vitamin A in a rat model of colitis to elucidate a possible mechanism of action. METHODS: Male rats were fed for 21 d with either a normal diet or high vitamin A diet (5000 IU/d). On day 22, colitis was induced with 2,4,6-trinitrobenzenesulfonic acid (TNBS). Rats were sacrificed after 24 h and colonic tissue was removed for evaluation. RESULTS: Morphologically, in the supplemented group preservation of tissue architecture, no vasculitis or necroses were detected. Biochemically, decreased myeloperoxidase activity and protection of the mitochondria as evaluated by preserving tissue oxygen consumption, mitochondrial DNA, and expression of cytochrome c, was observed. Vitamin A supplementation also increased the levels of nuclear respiratory factor (NFR)-1 and mitochondrial transcription factor-A (TFAM) in normal colon tissue and in colon tissue under inflammatory conditions. CONCLUSION: The results indicate that tissue damage in colitis is accompanied by the arrest of mitochondrial respiration, loss of mitochondrial DNA, and the expression of mitochondrial proteins. Vitamin A effectively protects colon mitochondria by upregulation of mitochondrial transcription factors, NFR-1 and TFAM, and prevents inflammatory and necrotic changes in colitis. Vitamin A is therefore a potential therapeutic agent in inflammatory bowel disease.

α-Linolenic acid (ALA) is an anti-inflammatory agent in inflammatory bowel disease.

Studies suggest that consumption of omega-3 (n-3) polyunsaturated fatty acids (PUFA) plays a protective role in inflammatory bowel disease; however, the use of plant-derived oils rich in α-linolenic acid (ALA) has not been widely investigated. The aims of this study were to test the effects of two different sources of (n-3) PUFA, fish and plant-derived oils, in two animal models of experimental colitis and to determine whether the (n-3) PUFA-enriched diets could ameliorate the inflammatory status. Rats were fed diets rich in corn, fish or sage oil with or without vitamin A supplementation for 3weeks then colitis was induced by adding dextran sodium sulfate to the drinking water or by injecting 2,4,6-trinitrobenzene sulfonic acid. We show that colitic rats fed the sage oil diets had a lower inflammatory response, improved histological repair and had less necrotic damage in the mucosa when compared to the corn and fish oil groups. Colonic damage and myeloperoxidase activity were significantly lower. Colonic mRNA levels of pro-inflammatory genes including interleukin IL-6, cyclooxygenase 2 and tumor necrosis factor α were markedly down-regulated in rats fed fish and sage oils compared to control. These results were supported by experiments in the human colonic epithelial cell line Caco-2, where ALA supplementation was shown to be effective in inhibiting inflammation induced by IL-1ß by down-regulating mRNA levels of pro-inflammatory genes including IL-8, COX2 and inducible nitric oxide synthase. Taken together, these results suggest that plant-derived oil rich in ALA could ameliorate the inflammatory damage in colitis.

Elevated milk ß-carotene and lycopene after carrot and tomato paste supplementation.

OBJECTIVES: To measure concentrations of ß-carotene and lycopene in the breast milk of healthy, well-nourished, lactating women supplemented with fresh carrot or tomato paste. METHODS: Twelve women were given fresh carrot paste and another 14 were given fresh tomato paste once a day for 3 d with a high-lipid-content meal. The women were instructed to avoid any food containing ß-carotene or lycopene, other than the test meal. Milk carotenoid levels were measured before, during, and after the trial. The carrot and tomato meals contained 15 mg of all-trans ß-carotene and 15 mg of all-trans lycopene, respectively. RESULTS: We demonstrated a significant increase in milk ß-carotene and elevated milk lycopene levels after the lipid-rich fresh carrot and tomato meals, respectively. CONCLUSIONS: We suggest that breast milk carotenoid levels reflect the mother's level of intake and can thus be raised by simple nutritional intervention. The results of this study may be relevant to breast-feeding mothers of both preterm and term infants by raising antiinflammatory and antioxidant properties in their milk.

ß-Carotene can reverse dysregulation of iron protein in an in vitro model of inflammation.

Anemia of chronic disease is frequently seen in chronic inflammatory conditions. Its hallmark is disrupted iron homeostasis, with increased uptake and retention of iron in cells of the reticuloendothelial system. Using the Caco-2 cell line as an in vitro model for iron absorption, local intestinal iron-related protein dynamics were evaluated during interleukin (IL)1ß/iron-induced inflammation, confirmed by IL8 release, and following ß-carotene and vitamin A supplementation. Time- and dose-dependent iron administration to the cells was then studied. The effects on heavy and light ferritin, ferroportin, transferrin receptor and intracellular iron levels were compared in inflamed Caco-2 cells with and without application of the anti-inflammatory agents ß-carotene and vitamin A. IL1ß treatment led to IL8 release, a surge in both ferritins' expressions and suppression of ferroportin and transferrin receptor expression. ß-Carotene significantly reduced IL8 (1,306.2-253.75 pg/ml), decreased light and heavy ferritin by 77.8 and 45.8%, respectively, and increased ferroportin by 59.9% (P < 0.05). Increasing iron concentrations and incubation periods resulted in increased IL8 release. A strong correlation was found between the levels of IL8 and the ferritins. Intracellular iron sequestration was induced by IL1ß and iron and alleviated by ß-carotene. ß-Carotene normalized the main iron-related proteins' levels, reduced IL8 production, and released intracellular trapped iron. These results highlight local mucosal control of iron regulation and suggest that by applying anti-inflammatory compounds, less iron is locked in inflamed intestinal epithelial cells, leading to its increased bioavailability. This suggests a possible approach to combating anemia associated with chronic inflammatory conditions.

The potential use of chickpeas in development of infant follow-on formula.

BACKGROUND: Undernutrition during childhood is a common disorder in the developing countries, however most research has focussed much on its treatment rather than its prevention. OBJECTIVE: We investigated the potential of using chickpeas in infant follow-on formula production against the requirements of WHO/FAO on complementary foods and EU regulations on follow-on formula. METHODS: Chickpeas were germinated for 72 hours followed by boiling, drying and dehulling in order to minimise associated anti-nutrition factors. Saccharifying enzymes were used to hydrolyse starch to maltose and the resulting flours were analysed for their protein content and amino acid profile. RESULTS: The protein content (percentage) increased from 16.66 ± 0.35 and 20.24 ± 0.50 to 20.00 ± 0.15 and 21.98 ± 0.80 for the processed desi and kabuli cultivar compared to raw chickpeas, respectively (P < 0.05). There was insignificant change (P = 0.05) in amino acid profile following processing and the resulting flour was found to meet the amino acid requirements of WHO/FAO protein reference for 0-24 month's children. CONCLUSION: The designed chickpea based infant follow-on formula meets the WHO/FAO requirements on complementary foods and also the EU regulations on follow-on formula with minimal addition of oils, minerals and vitamins. It uses chickpea as a common source of carbohydrate and protein hence making it more economical and affordable for the developing countries without compromising the nutrition quality.

Membrane lipid modification by polyunsaturated fatty acids sensitizes oligodendroglial OLN-93 cells against oxidative stress and promotes up-regulation of heme oxygenase-1 (HSP32).

Polyunsaturated fatty acids (PUFA) are highly abundant in brain tissue, and docosahexaenoic acid (DHA) might protect cells from oxidative stress (OS) during inflammation and demyelinating disorders, but also might exert pro-oxidant effects. Here we investigated if PUFA supplements lead to heat shock protein induction, altered cell survival properties and stress responses to OS exerted by hydrogen peroxide in oligodendroglial OLN-93 cells. The data show that supplements of various fatty acids (FA) with 18-22 carbons chain length and 2-6 double bonds led to PUFA enrichment in cellular membranes. Depending on the degree of desaturation, FA-supplements caused the up-regulation of heme oxygenase-1 (HSP32), a stress protein inducible by OS, and an increase in sensitivity to hydrogen peroxide-treatment. DHA, with the highest number of double bonds, was most effective. Co-treatment with DHA and the lipophilic vitamin E analogue alpha-tocopherol, suppressed heme oxygenase-1 up-regulation and cell survival was restored. Analysis of the lipid profile demonstrates that alpha-tocopherol not only has antioxidant capacities, but also directly modified the PUFA profile in cell membranes. Enrichment with higher omega-3, -6 and -9 PUFA and an increase in the biosynthesis rate of very long chain fatty acids, mainly changed the FA profile of ethanolamine and serine phosphoglycerides.

Effect of music by Mozart on energy expenditure in growing preterm infants.

OBJECTIVE: The rate of weight gain in preterm infants who are exposed to music seems to improve. A potential mechanism could be increased metabolic efficiency; therefore, we conducted this study to test the hypothesis that music by Mozart reduces resting energy expenditure (REE) in growing healthy preterm infants. DESIGN. A prospective, randomized clinical trial with crossover was conducted in 20 healthy, appropriate-weight-for-gestational-age, gavage-fed preterm infants. Infants were randomly assigned to be exposed to a 30-minute period of Mozart music or no music on 2 consecutive days. Metabolic measurements were performed by indirect calorimetry. RESULTS: REE was similar during the first 10-minute period of both randomization groups. During the next 10-minute period, infants who were exposed to music had a significantly lower REE than when not exposed to music (P = .028). This was also true during the third 10-minute period (P = .03). Thus, on average, the effect size of music on REE is a reduction of approximately 10% to 13% from baseline, an effect obtained within 10 to 30 minutes. CONCLUSIONS: Exposure to Mozart music significantly lowers REE in healthy preterm infants. We speculate that this effect of music on REE might explain, in part, the improved weight gain that results from this "Mozart effect."

Sub-occipital craniectomy in a lion (Panthera leo) with occipital bone malformation and hypovitaminosis A.

Neurologic dysfunction accompanied by malformation of both the skull and the cervical vertebrae has been previously described in lions kept in captivity worldwide, and this dysfunction and malformation were most often related to vitamin A deficiency. Diagnosis of the bone malformation and its effects on the neural tissue was until recently limited to postmortem examination, with characteristic thickening of the bones of the cranial vault, cerebellar herniation, compression of the foramen magnum, and enlargement of the lateral ventricles. For some mildly affected lion cubs with neurologic signs, improvement was reported with excessive vitamin A supplementation. However, definitive diagnosis was only available for those that eventually died or were euthanized. This case documents the antemortem diagnosis of the disease using computed tomographic imaging and liver biopsy. While conservative treatment failed, suboccipital craniectomy removed the thickened occipital bone and was demonstrated to be a successful surgical intervention that can be used to treat more severely affected lions.

High selenium diet protects against TNBS-induced acute inflammation, mitochondrial dysfunction, and secondary necrosis in rat colon.

OBJECTIVE: We studied the protective effects of selenium in a rat model of 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis to elucidate a possible mechanism of action. METHOD: Rats were supplemented with sodium selenite for 21 d with a normal selenium diet (0.02 microg/g body weight), an intermediate selenium diet (ISD; 0.3 microg/g body weight), or a high selenium diet (HSD; 2 microg/g body weight). On day 22, colitis was induced with TNBS. Rats were sacrificed after 24 h and colonic tissue was removed for evaluation. RESULTS: Selenium supplementation (HSD) resulted in a significant increase in selenium in colonic tissue. Morphologically, the HSD resulted in the preservation of tissue architecture and attenuated neutrophil infiltration; no vasculitis or necrosis was detected. Biochemically, the HSD decreased tissue myeloperoxidase activity and protected the mitochondria in the colon of TNBS-treated animals as evaluated by preserving tissue oxygen consumption, mitochondrial DNA, and expression of cytochrome c. The HSD increased levels of nuclear respiratory factor-1 and mitochondrial transcription factor-A in normal colon tissue and under inflammatory conditions. The ISD resulted in only a minor protective effect. CONCLUSION: The results indicate that tissue damage in TNBS-induced colitis is accompanied by the arrest of mitochondrial respiration, loss of mitochondrial DNA, and the expression of nuclear-encoded mitochondrial proteins. Selenium effectively protects colon mitochondria by upregulation of the expression of mitochondrial transcription factors nuclear respiratory factor-1 and mitochondrial transcription factor-A. Selenium prevented inflammatory and necrotic changes after induction of colitis. Selenium in a high dose is therefore a potential therapeutic agent in inflammatory bowel disease.

Weight gain reduction in mice fed Panax ginseng saponin, a pancreatic lipase inhibitor.

Roots of the herb Panax ginseng are known to contain high levels of bioactive saponins. Here, we isolated saponins from ginseng root powder and studied their inhibitory effect on the absorption of dietary fat in male Balb/c mice. Consumption of ginseng saponins suppressed the expected increase in body weight and plasma triacylglycerols, following a high-fat diet and observed higher intake. Consumption of ginseng saponins had no effect on the concentration of the total plasma cholesterol in both chow and high-fat diets in mice. The mode by which saponins from ginseng inhibit lipid metabolism was assessed as the in vitro inhibition of pancreatic lipase. Ginseng saponin inhibited pancreatic lipase with an apparent IC50 value of 500 mug/mL. Our results suggest that the anti-obesity and hypolipidemic effects of Ginseng in high-fat diet-treated mice were attributed to the isolated saponin fraction. These metabolic effects of the ginseng saponins may be mediated by inhibition of pancreatic lipase activity.

Effect of nutrition on growth in short stature before and during growth-hormone therapy.

OBJECTIVE: Although nutritional counseling is an integral part of the management of rapidly growing children, few studies have focused on the importance of nutritional supervision during growth-hormone (GH) therapy. The objective of this study was to study the effect of caloric intake on growth before and during GH therapy. METHODS: A total of 115 short normal prepubertal children who were 7.4 +/- 1.2 years of age (mean +/- SD) and had height SD score (SDS) of -2.5 +/- 0.6 were treated with a GH dose range of 0.13 to 0.52 mg/kg per week for 1 year. A 3-day nutritional recall and blood chemistry analysis were repeated every 3 months. RESULTS: Caloric intake (expressed as % recommended dietary allowance) was positively correlated with the pretreatment growth velocity (SDS) and the increment in growth velocity SDS during the first year of GH therapy (r = 0.363 and 0.493). By stepwise regression analysis, we identified 4 parameters that could predict the 1-year increment in growth velocity SDS: the contribution of each factor (% variability) was pretreatment growth velocity SDS 36%, GH dose (27%), caloric intake 4%, and the integrated concentration of GH 2% (r(2) = 0.689). GH therapy induced an alkaline phosphatase increment of 59 +/- 49 IU/mL, an insulin-like growth factor-I increment of 32.6 +/- 11.9 nmol/L, and a GH binding protein increment of 10.2 +/- 2.7%. During GH therapy, an increase in serum transferrin (56.5 +/- 35.2 mg/dL) and a decrease in serum iron (20.5.5 +/- 20.2 microg/dL) were noted. These changes could not be detected through hemoglobin levels or hematopoietic indexes. Dietary iron supplementation reversed this phenomenon. CONCLUSIONS: The nutritional status of GH-treated patients before and throughout the course of GH treatment should be monitored closely to improve the growth response and prevent nutritional deficiencies. Special emphasis should be placed on iron nurture.

Vitamin A exerts its activity at the transcriptional level in the small intestine.

THE AIM OF THIS STUDY: was to examine the effects of vitamin-A deficiency on the small intestinal morphology and on brush-border enzyme function and expression. METHODS: Weanling male rats were fed a vitamin-A deficient (VAD), sufficient (VAS), or supplemented (VASUP) diet, or were pair-fed (PF) with the VAD rats. Average food intakes were not different among the groups. RESULTS: From days 35 to 42, the body weight of VAD rats began to plateau, whereas the other groups, including the PF rats, continued to gain weight. At days 48 to 51, the final mean body weight of VAD rats was significantly lower than that of PF, VAS and VASUP rats (P < 0.05). Serum and liver retinol levels were lower in VAD rats (by 85 % and 99%, respectively) and higher in the VASUP group (by 126 % and 160%, respectively) compared to the VAS group (P < 0.01). Histological examination of the jejunum revealed that in VAD rats the villi were shorter and thicker and there was an elevation in crypt depth relative to the other treatment groups. Infiltration of inflammatory cells was also observed in the jejunum of most of the VAD rats, but not in rats from other groups. Biochemical assays revealed that in VAD rats, alkaline phosphatase (ALP) and sucrase-isomaltase (SI) activities are significantly decreased in the jejunum, compared to PF, VAS and VASUP groups (P < 0.01). ALP activity was decreased in the duodenum of VAD rats as well. By comparison, amino-peptidase (AP) activity per mg protein in the jejunum and ileum of VAD rats was significantly increased compared to VAS and VASUP rats (P < 0.01), but was not different from PF rats. In all of the small intestinal sections, mRNA expression of all three brush-border enzymes relative to beta-actin were significantly lower in VAD rats than in the other treatment groups. SI was similarly expressed in all of the small intestinal organs, whereas AP and ALP expression varied. CONCLUSIONS: Our results suggest that vitamin-A deficiency modifies the maturation and differentiation processes of the small intestinal mucosa at the transcriptional and post-transcriptional levels respectively. This in turn may be one explanation for the alteration or elimination of nutrient digestion and absorption during VAD.

Dietary iron affects inflammatory status in a rat model of colitis.

Iron deficiency anemia is a common feature in inflammatory bowel disease, and oral supplementation is one of the mainstay therapies. However, there is some concern that oral iron supplementation may lead to oxidative stress and exacerbation of inflammation. Our objective was to study the effect of severely deficient, moderately deficient, normal and high iron status on oxidative stress and the course of inflammation in a rat model of colitis induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS). The rats were randomly assigned to receive the low-iron diet for 3 (moderately iron-deficient group, n = 16) or 5 (severely iron-deficient group, n = 16) wk, the normal iron diet for 2 wk (normal iron group, n = 16) or the high-iron diet for 2 wk (high-iron group, n = 16). Malondialdehyde concentration, electroparamagnetic resonance measurement, myeloperoxidase activity, and histological analysis were used to evaluate oxidative stress. Noncolitic rats in the high-iron group had higher oxidative stress parameters than those in the other groups. The induction of colitis resulted in severe inflammatory changes in the high-iron and severely iron-deficient groups, and produced higher histological scores in the colon of the normal and high-iron groups. Iron overload, oxidative stress, and inflammation were lower in the moderately iron-deficient group compared with the other 3 groups. In conclusion, we suggest that low rather than normal or high iron supplementation should be considered for the treatment of iron deficiency in inflammatory bowel disease.

5-ASA and lycopene decrease the oxidative stress and inflammation induced by iron in rats with colitis.

BACKGROUND: Supplementation of 5-aminosalicylic acid (5-ASA) and of iron are among the principal therapies in patients with inflammatory bowel disease. Therapeutic iron, as well as heme iron from chronic mucosal bleeding, can increase iron-mediated oxidative stress in colitis. This study was designed to examine the influence of iron supplementation on histological expression and oxidative status relative to 5-ASA treatment and antioxidant treatment. METHODS: Colitis was induced using the iodoacetamide rat model, and rats were divided into different dietary groups of 6 rats each: 1, normal chow diet (control); 2, diet supplemented with iron; 3, iron supplementation and lycopene; 4, iron and Beta-carotene; 5, 5-ASA; 6, 5-ASA and lycopene; 7, 5-ASA and iron; 8, 5-ASA, iron, and lycopene. The animals were killed after 3 days and the weight of the ulcerated area recorded. Mucosal specimens were histologically evaluated. Myeloperoxidase (MPO) was measured to evaluate inflammatory status (U/g). Malondialdehyde (MDA) was measured in colonic tissue ( micro mol/g) and superoxide dismutase (SOD) in erythrocytes to assess the degree of tissue oxidative stress. RESULTS: Significantly more severe colitis, including necrosis, ulceration, and hemorrhage, was seen in colonic biopsies of rats with colitis when iron was supplemented. This pathology was attenuated when iron was given in combination with 5-ASA and/or lycopene. There was no significant benefit from adding Beta-carotene. CONCLUSIONS: Iron supplementation can amplify the inflammatory response and subsequent mucosal damage in a rat model of colitis. We suggest that the resultant oxidative stress generated by iron supplementation leads to the extension and propagation of crypt abscesses, either through direct membrane disruption by lipid peroxidation or through the generation of secondary toxic oxidants. Simultaneous treatment with 5-ASA and/or lycopene minimizes the potential hazard of iron. Therefore, we suggest giving iron supplementation with 5-ASA or lycopene or both.