Cytokine distribution in mothers and breastfed children after omega-3 LCPUFAs supplementation during the last trimester of pregnancy and the lactation period: A randomized, controlled trial.

OBJECTIVE: To determine whether maternal diet supplementation with omega-3 long chain polyunsaturated fatty acids (omega-3 LC-PUFAs) during the last trimester of pregnancy and the breastfeeding period influences the levels of inflammatory cytokines in mother and infants. MATERIAL AND METHOD: This registered, double-blind randomized study included 46 pregnant women, who were randomly allocated to either an experimental group receiving 400mL/day of a fish oil-enriched dairy drink [320mg docosahexaenoic acid (DHA) + 72mg eicoapentaenoic acid] (FO group, n = 24) or to a control group receiving 400mL/day of a non-supplemented dairy drink (CT group, n = 22), from week 28 of pregnancy until the fourth month of lactation. During the study, maternal dietary patterns were monitored by a nutritionist, who encouraged compliance with current recommendations of fatty acids intake. DHA concentrations and cytokine levels (GM-CSF, IL-2, IL-4, IL-6, IL-10, INF-γ and TNF-α) were measured in maternal plasma at the moment of recruitment and in maternal (n = 46) and infant (n = 46) plasma at birth and 2.5 months after birth. RESULTS: Maternal plasmatic IL-4 levels were higher in FO than in CT subjects (p = 0.009). Additionally, a tendency was observed to higher IL-10 and IL-2 in the FO group. Plasmatic IL-6 however, was higher in CT mothers (p = 0.001). TNF-α was higher in CT infants at birth and 2.5 months after birth (p = 0.005). An analysis of possible relationships between DHA and the concentrations of different cytokines revealed negative correlation between maternal plasmatic IL-6 and DHA (higher plasmatic DHA corresponded to lower IL-6). CONCLUSIONS: Maternal dietary omega-3 LC-PUFAs supplementation during critical periods like pregnancy, lactation and early newborn development may influence the levels of certain inflammatory cytokines, reducing pro-inflammatory cytokines and promoting an anti-inflammatory "environment".

The Benefits of Administering Folic Acid in Order to Combat the Oxidative Damage Caused by Binge Drinking in Adolescent Rats.

AIMS: An important mechanism in alcohol-induced injury is biomolecular oxidative damage. Folic acid is supplied to chronic alcoholic patients in order to prevent this situation, as this is the main vitamin deficiency that they suffer from. Acute alcohol exposure, such as binge drinking, is one of the most widespread ethanol consumption models practiced by adolescents. However, there is no evidence of folic acid body profiles after this pattern of consumption. METHODS: Four groups of adolescent rats were used: control, alcohol (exposed to intraperitoneal binge drinking), control folic acid-supplemented group and alcohol folic acid-supplemented group. Folic acid levels, protein, lipid and DNA oxidative damage in serum, and liver glutathione (GSH) and reduced/oxidized glutathione ratio (GSH/GSSG) were measured. RESULTS: Binge-drinking rats had higher lipids and DNA oxidation levels. They also had lower hepatic GSH levels and GSH/GSSG ratio. Folic acid supplementation to binge-drinking rats does not change the serum protein oxidation but decreases lipid and DNA oxidation. Finally, GSH increased to control levels with folic acid supplementation. CONCLUSION: Folic acid supplementation is an economic and efficient therapy against the oxidative damage in lipids and mainly in DNA stability caused by binge drinking during adolescence. It has also been demonstrated that folic acid increases GSH levels, improving the antioxidant status and revealing a hepatoprotective effect during binge drinking.

Advantages and disadvantages of the animal models v. in vitro studies in iron metabolism: a review.

Iron deficiency is the most common nutritional deficiency in the world. Special molecules have evolved for iron acquisition, transport and storage in soluble, nontoxic forms. Studies about the effects of iron on health are focused on iron metabolism or nutrition to prevent or treat iron deficiency and anemia. These studies are focused in two main aspects: (1) basic studies to elucidate iron metabolism and (2) nutritional studies to evaluate the efficacy of iron supplementation to prevent or treat iron deficiency and anemia. This paper reviews the advantages and disadvantages of the experimental models commonly used as well as the methods that are more used in studies related to iron. In vitro studies have used different parts of the gut. In vivo studies are done in humans and animals such as mice, rats, pigs and monkeys. Iron metabolism is a complex process that includes interactions at the systemic level. In vitro studies, despite physiological differences to humans, are useful to increase knowledge related to this essential micronutrient. Isotopic techniques are the most recommended in studies related to iron, but their high cost and required logistic, making them difficult to use. The depletion-repletion of hemoglobin is a method commonly used in animal studies. Three depletion-repletion techniques are mostly used: hemoglobin regeneration efficiency, relative biological values (RBV) and metabolic balance, which are official methods of the association of official analytical chemists. These techniques are well-validated to be used as studies related to iron and their results can be extrapolated to humans. Knowledge about the main advantages and disadvantages of the in vitro and animal models, and methods used in these studies, could increase confidence of researchers in the experimental results with less costs.

The effects of ethanol upon hydric balance and arterial pressure in rats: folic acid as a possible hypotensor.

AIMS: Chronic alcohol intake is related to hypertension. There are, however, few studies concerning the effect of ethanol upon hydric balance in relation to arterial pressure. Folic acid intake has beneficial effects upon the cardiovascular system decreasing hyperhomocysteinemia, however, more studies imply that it is related with other mechanisms. Therefore, we have studied the effects of chronic alcohol intake (30% v/v) upon hydric-saline balance and hypertension and have found that dietary supplementation with folic acid (8 mg/kg) improves the above parameters. MAIN METHODS: Our study used four experimental groups of rats: control, alcohol, alcohol with folic acid and control with folic acid. In all cases we measured the clearance of Na(+), K(+) and aldosterone; osmolarity in urine, liquid and solid ingestion; homocysteine levels in serum; cardiac frequency and arterial blood pressure. KEY FINDINGS: The alcohol intake increases serum aldosterone and homocysteine, which is reflected in an increase in arterial blood pressure. In addition, we have found that alcohol intake reduces both liquid and solid ingestion (causing a malnourishment status), the clearance of creatinine, aldosterone, Na(+) and K(+), and the ratio ClNa(+)/ClCr; it also increases urine osmolarity. Folic acid supplementation increases the clearance of Na(+) and the ratio ClNa(+)/ClCr. SIGNIFICANCE: Folic acid intake improves the hypertension provoked by alcohol by increasing the aldosterone clearance, drastically reducing the serum levels of this hormone and thus its hypertensor effect.

Goat milk during iron repletion improves bone turnover impaired by severe iron deficiency.

The effect of goat or cow milk-based diets, with either normal Fe content or an Fe overload, on bone turnover and the mineralization process was studied in control and anemic rats during chronic Fe repletion. One hundred eighty male Wistar rats were studied during a pre-experimental period of 40 d in which they were randomly divided into 2 groups, a control group receiving the AIN-93G diet with normal Fe content (45 mg/kg of diet) and the Fe-deficient group receiving the AIN-93G diet with low Fe content (5mg/kg of diet) for 40 d. After the pre-experimental period, the rats were fed for 10, 30, or 50 d with goat or cow milk-based diets with a normal Fe content (45 mg/kg of diet) or an Fe overload (450 mg/kg of diet). In anemic rats, goat milk with normal Fe content increased levels of the biomarker of bone formation N-terminal propeptides of type I procollagen and diminished parathyroid hormone levels after only 10 d of supplying this diet, indicating the beginning of restoration of the bone demineralization induced by the anemia, which was not observed with cow milk. After 30 d of supplying the milk-based diets with normal Fe content or an Fe overload, biomarkers of bone formation and bone resorption were not different between control and anemic rats, indicating that the bone demineralization induced by the Fe-deficiency anemia had recovered, although the process of stabilization of bone turnover began earlier in the animals fed goat milk. In addition, a higher Ca deposit was observed in femur, which positively affects bone mineralization, as well as an increase of Fe in sternum, which indicates that the hematopoietic process essentially recovered earlier on the goat milk diet compared with the cow milk diet.

Utilización nutritiva de fósforo en el transcurso de la anemia ferropénica nutricional / Nutritive utilization of phosphorus during the course of nutritional ferropenic anaemia

Se ha estudiado el efecto de la evolución de la anemia ferropénica nutricional sobre la utilización digestiva y metabólica de fósforo en tres periodos 20, 30 y 40 días. Los animales de experimentación han sido 48 ratas macho de la raza Wistar albina que se dividieron en 6 grupos: tres grupos controles(C) y tres grupos ferrodeficientes (FD) que recibieron una dieta AIN 93G con contenido normal (45mg Fe/kg dieta) o con un bajo contenido de hierro (5 mg/Fe Kg dieta) respectivamente durante 20, 30 ó 40 días. Se ha encontrado un aumento significativo en la utilización digestiva y metabólica de fósforo en el transcurso de la anemia ferropénica nutricional, efecto que se va haciendo más patente a medida que evoluciona la ferrodeficiencia. Este incremento en la utilización nutritiva de fósforo es debido principalmente al mecanismo pasivo de absorción de fósforo que opera principalmente en el yeyuno-íleon y es predominante en situación de anemia ferropénica nutricional(AU)

The evolution of the nutritional iron deficiency anemia on the digestive and metabolic utilization of phosphorus has been studied during three periods: 20, 30 and 40 days. 48 male Wistar albino breedrats were divided in 6 groups: three control groups (C) and three Fe-deficient groups (FD) receiving AIN 93G with normal-Fe content (45 mg /kg diet) or with a low-Fe content (5 mg/Kg diet) respectively during 20, 30 ó 40 days. A significant increase in the digestive and metabolic utilization of phosphorus has been found in the course of the nutritional iron deficiency anemia, effect that become more pronounced as the ferrodeficiency is instaured. This increase in the nutritive utilization of phosphorus is due mainly to the passive mechanism of phosphorus absorption which operates principally in the jejunum-ileum and is predominant in situation of nutritional iron deficiency anemia(AU)

Relación hepatosomática y depósito de hierro en hígado durante la instauración de anemia ferropénica nutricional / Hepatosomatic index and iron liver stores during the instauration of nutritional ferropenic anaemia

El hígado es el principal órgano de almacén de hierro en el organismo y juega un papel crucial en la homeostasis de dicho mineral. Los niveles de hierro en se consideran un fiel reflejo del estatus de hierro en el organismo, hecho que nos indujo a determinar la relación hepatosomática y el contenido de hierro en hígado durante la instauración de la anemia ferropénica nutricional inducida experimentalmente en ratas en crecimiento. Los depósitos de hierro estaban profundamente deplecionados, el peso corporal y el peso hepático fue menor en animales anémicos. Como consecuencia, la relación hepatosomática se incrementó en animales ferrodeficientes. Durante la ferrodeficiencia, varios factores reguladores de la hepcidina se alteran, aumenta la demanda eritropoyética por disminución de los parámetros hematológicos, hay un menor aporte de oxígeno a los tejidos y se deplecionan los depósitos corporales, alterándose el metabolismo de hierro, hechos que conducen a una disminución de dicha hormona, lo cual se traducirá en una menor interacción con la ferroportina 1, evitando su internalización y degradación, de manera que aumenta el flujo de salida de hierro ferroso desde los hepatocitos y consecuentemente se reduce su depósito. Por otra parte, la ferrodeficiencia afectó el peso corporal, hecho que se puede atribuir a los menores niveles de hormonas tiroideas encontrados en esta patología. Puesto que hay una clara reducción de la hemoglobina y recuento de hematíes, el suministro de oxígeno a las células se limita considerablemente e incide negativamente en la síntesis de ATP e incremento de peso(AU)

Liver is main storage organ of iron in the organism and plays a crucial role in the homeostasis of this mineral. The levels of iron are considered a routine index of the iron status in the body, fact that encouraged us to asses the hepatosomatic index and the iron content in liver, during iron-deficiency anaemia in growing rats. In rats with iron-deficiency anaemia, iron deposits were deeply depleted, body weight and hepatic weight were lower, moreover the hepatic iron deposits were lower in anaemicrats. During the iron-deficiency, several regulatory factors of the hepcidin are impaired (the erythropoietic demand increase due to the decrease of the haematological parameters, there is a minor supply of oxygen to the tissues and the body stores are depleted, being the iron metabolism altered), facts that leads to a decrease of the above mentioned hormone, which will be translated in a minor interaction with the ferroportin1, avoiding its internalization and degradation, therefore increases the outflow of ferrous iron from the hepatocytes and consistently its storage diminishes in the above mentioned organ. On the other hand, the iron-deficiency impaired the body weight, fact that can be related with the lower levels of thyroid hormones found in this pathology. Moreover, since in iron deficiency situation the haemoglobin and red blood cells count diminish drastically, the supply of oxygen to the cells limits itself considerably, which affects in a negative way to the ATP synthesis andincrease of weight(AU)