Metabolic syndrome during gestation and lactation: An important renal problem in dams. selenium renal clearance.

BACKGROUND: Metabolic syndrome (MS) in lactating dams leads to several cardiometabolic changes related to selenium (Se) status and selenoproteins expression which produce hypertension. However, little is known about the state of these dams' kidney functions and their Se deposits. METHODS: Two experimental groups of dam rats were used: control (Se: 0.1 ppm) and MS (Fructose 65 % and Se: 0.1 ppm). At the end of lactation (21d postpartum) kidney weight and protein content, Se deposits, and the activity of the antioxidant selenoprotein glutathione peroxidase (GPx) were measured in dams. Kidney functional parameters: albuminuria, creatinine clearance, serum aldosterone and uric acid levels and water and electrolyte (Na+ and K+) balance were also evaluated. Systolic blood pressure (SBP) was measured. RESULTS: In MS dams at the end of lactation Se deposits and GPx activity are higher in the kidney; however, lipid renal peroxidation appears, relative Se clearance increases, and the dams have lost Se by urine. MS dams have polyuria and polydipsia, high uric acid serum levels, albuminuria and high creatinine clearance, implying glomerular renal malfunction with protein loss. They also present hypernatremia, hypokalemia and hyperaldosteronemia, leading to high SBP; however, a natriuretic process is taking place. CONCLUSION: Since these alterations appear, at least in part, to be related to oxidative stress in renal cells, Se supplementation could be beneficial to avoiding greater lipid renal oxidation during lactation.

Upper deep venous thrombosis secondary to biceps brachii tear: A clinical case. / Trombosis venosa profunda del miembro superior secundaria a rotura musculotendinosa del bíceps braquial: a propósito de un caso clínico.

We describe an unusual case of axillary vein thrombosis after extensive muscular and fibrillar rupture of the long tendon of the right biceps brachii in a 43-year-old patient after an effort. The difficult diagnosis of this condition requires high suspicion and early treatment.

Detection of pathogenic Leptospira species associated with phyllostomid bats (Mammalia: Chiroptera) from Veracruz, Mexico.

The genus Leptospira encompass 22 species of spirochaetes, with ten pathogenic species that have been recorded in more than 160 mammals worldwide. In the last two decades, the numbers of records of these agents associated with bats have increased exponentially, particularly in America. Although order Chiroptera represents the second most diverse order of mammals in Mexico, and leptospirosis represents a human and veterinary problem in the country, few studies have been conducted to identify potential wildlife reservoirs. The aim of this study was to detect the presence and diversity of Leptospira sp. in communities of bats in an endemic state of leptospirosis in Mexico. During January to September 2016, 81 bats of ten species from three localities of Veracruz, Mexico, were collected with mist nets. Kidney samples were obtained from all specimens. For the detection of Leptospira sp., we amplified several genes using specific primers. Amplicons of the expected size were submitted to sequencing, and sequences recovered were compared with those of reference deposited in GenBank using the BLAST tool. To identify their phylogenetic position, we realized a reconstruction using maximum-likelihood (ML) method. Twenty-five samples from three bat species (Artibeus lituratus, Choeroniscus godmani and Desmodus rotundus) showed the presence of Leptospira DNA. Sequences recovered were close to Leptospira noguchii, Leptospira weilii and Leptospira interrogans. Our results include the first record of Leptospira in bats from Mexico and exhibit a high diversity of these pathogens circulating in the state. Due to the finding of a large number of positive wild animals, it is necessary to implement a surveillance system in populations of the positive bats as well as in related species, in order to understand their role as carriers of this bacterial genus.

Changes in the Fatty Acid Profile and Phospholipid Molecular Species Composition of Human Erythrocyte Membranes after Hybrid Palm and Extra Virgin Olive Oil Supplementation.

This work aims to evaluate and compare, for the first time, the effects of extra virgin olive oil (EVOO) and hybrid palm oil (HPO) supplementation on the fatty acid profile and phospholipid (PL) molecular species composition of human erythrocyte membranes. Results supported the effectiveness of both HPO and EVOO supplementation (3 months, 25 mL/day) in decreasing the lipophilic index of erythrocytes with no significant differences between HPO and EVOO groups at month 3. On the other hand, the novel and rapid ultraperformance liquid chromatography-tandem mass spectrometry method used for PL analysis reveals an increase in the levels of phosphatidylcholine and phosphatidylethanolamine species esterified with polyunsaturated fatty acids. This work demonstrates the ability of both EVOO and HPO to increase the degree of unsaturation of erythrocyte membrane lipids with an improvement in membrane fluidity that could be associated with a lower risk of developing cardiovascular diseases.

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.

Oxidative effects of chronic ethanol consumption on the functions of heart and kidney: folic acid supplementation.

AIMS: The principal aim of this study was to investigate the oxidative effects of chronic ethanol consumption on the functions of the heart and the kidney and the possible modification of this effect by folic acid supplementation. Moreover, in order to find whether this oxidative profile affects cardiovascular function, parameters such as heart rate and glomerular filtration rate were also assessed. METHODS: Four experimental groups of rats were used: control, ethanol-exposed, control supplemented with folic acid and ethanol-exposed plus folic acid. Ethanol-exposed rats were subjected to a chronic ethanol treatment (2 months), in which the level of alcohol reaches 30% v/v. Diet and ethanol solution were provided ad libitum, and folic acid supplementation was 8 vs. 2 ppm. Energy intake, creatinine clearance and heart rate were determined. Antioxidant enzyme activity and lipid and protein peroxidation of the kidney and the heart were measured by the spectrophotometric method. RESULTS: Ethanol increases heart size and catalase (CAT) activity and decreases lipid peroxidation in heart without changing heart rate. However, in the kidney, ethanol decreases CAT activity, increases lipid peroxidation and decreases glomerular filtration rate. Folic acid supplementation avoids these situations; it does not, however, improve glomerular function. CONCLUSION: Chronic ethanol consumption has many effects on the antioxidant enzymatic activity of the heart and the kidney, leading to increased renal lipid peroxidation prevented by folic acid supplementation.

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.

Effect of dietary selenite on development and intestinal absorption in offspring rats.

AIM: The present study aims to compare selenium (Se) status in offspring rats born to selenium-deficient and selenium supplemented dams and to analyse Se's influence on intestinal parameters and the intestinal absorption of selenomethionine (Se-Met). MAIN METHODS: Male and female Wistar rats (150-200 g) were randomised in: control (C) (0.1 ppm Se), Se-deficient (SD) (0.01 ppm Se) and Se-supplemented (SS) (0.5 ppm Se) groups; and were mated to obtain their offspring. Se levels in serum, urine and faeces in offspring and in mothers' milk were measured by graphite-furnace atomic absorption spectrometry. Duodenal transport studies in offspring were performed using an in vivo perfusion of different Se-Met concentrations (2, 5, 10, 25, 75 and 150 µM). KEY FINDING: A Se-deficient diet provoked a decrease in the offspring's body weight and intestinal parameters, while the supplemented diet increased these values. Serum Se levels were similar between Se-deficient and control offspring because the urinary excretion of Se was smaller to compensate for Se homeostasis. Intestinal Se-Met absorption obeys the Michaelis-Menten equation with lower apparent constant (K(m)) and maximal velocity (V(max)) in the SD group. However, the C and SS groups presented similar K(m) and different V(max). The V(max) showed greater values in the following order of rank: SS>C>SD groups. SIGNIFICANCE: Selenium intake deficiencies in offspring lead to the development of compensatory mechanisms in order to normalise serum selenium levels. These mechanisms, however, do not permit normal body development; nor do they regulate intestinal parameters and Se-Met transport.

Selenium or selenium plus folic acid intake improves the detrimental effects of ethanol on pups' selenium balance.

The levels of folic acid and selenium, two nutrients with antioxidant properties, decrease in dams exposed to ethanol during gestation and lactation. This decrease affects their antioxidant balance, and consequently the health of their offspring. In this study we have proved that a supplemented diet with Se (0.5 ppm) or with Se (0.5 ppm) plus folic acid (8 ppm) to ethanol-exposed (20%v/v) dams prevents the ethanol-provoked effects in their offspring's Se deposits. Se levels in milk, serum, urine, faeces and several tissues were measured by graphite-furnace atomic absorption spectrometry. Results show that ethanol decreases Se deposits in pups' heart, liver, kidney and testes. However Se levels in pancreas and in serum were increased by ethanol; it also compromised the weight and the length of the offspring at the end of lactation. Our supplemented diets to ethanol dams increased all of these impaired levels, and restored Se pancreas concentration to a control status. However Se-only therapy mainly displaces Se to serum, kidney and spleen, and co-treatment with Se plus folic acid, mainly displaces Se to liver and brain. This data demonstrate that the qualitative and quantitative Se organ deposits depend on ethanol consumption, Se status, and the presence of other antioxidants.

Dietary selenium plus folic acid as an antioxidant therapy for ethanol-exposed pups.

BACKGROUND: Nutrients such as folic acid and selenium are decreased in dams exposed to ethanol during gestation and lactation, affecting their metabolism, antioxidant balance, and the future health of their progeny. We will study whether the supplementation of the maternal diet with folate and selenium can prevent ethanol-induced oxidative liver disorders in the offspring. METHODS: Dams were randomised into four groups: control, alcohol, alcohol+folic acid+Se, and control+folic acid+Se. We determined selenium by graphite-furnace atomic absorption and antioxidant enzyme activities, lipid peroxidation, and protein carbonyl by spectrophotometry in the offspring. RESULTS: Alcohol increased serum Se levels and glutathione peroxidase (GPx) activity. However, in the liver of pups from ethanol-exposed dams a decrease in selenium was provoked and GPx activity increased with the double supplementation. Glutathione reductase (GR) and catalase (CAT) activities increased with ethanol, while double supplementation significantly decreased the GR activity. The supplemented diet reduced the protein peroxidation found in ethanol pups. CONCLUSIONS: These results suggest that folic acid+Se could be effective in neutralising the damage of ethanol consumption in pups since it prevents peroxidation protein products.

Selenium tissue distribution changes after ethanol exposure during gestation and lactation: selenite as a therapy.

Ethanol consumption affects maternal nutrition and antioxidant status together with the future health of their progeny. Selenium (Se) is a trace element with antioxidant activity; we will study the effect of ethanol in dams on Se bioavailability, antioxidant balance and gestational parameters. We also will study if a Se-supplemented diet (0.5 ppm) administered to ethanol-exposed dams avoids the undesirable effects provoked by ethanol. We have used four experimental groups: control (C); chronic ethanol (A); control+Se (CS) and chronic ethanol+Se (AS). Se levels in serum, urine, faeces, and several tissues were measured by graphite-furnace atomic absorption spectrometry. Serum glutathione peroxidase (GPx) activity was determined by spectrometry. Se bioavailability is altered by ethanol, causing a decrease in Se retention, reducing Se levels in cortex, muscle, mammary gland and salivary gland while elevating Se values in heart, liver and spleen. On the other hand, Se supplementation increases some of these parameters. Serum GPx activity was decreased by ethanol, while a Se-supplemented diet restores these values to those found in controls. We have demonstrated that ethanol decreased Se retention in dams, affecting their tissues' Se deposits, decreasing GPx activity in serum, gestational parameters and the weight of their progeny. Selenite supplementation counteracts these decreasing effects, except in cortex.

Effect of maternal ethanol consumption during pregnancy and lactation on kinetic parameters of folic acid intestinal transport in suckling rats.

Ethanol ingestion is known to interfere with folate absorption and metabolism. A fostering/crossfostering analysis of maternal ethanol exposure effects on jejunum and ileum kinetic parameters in vivo of offspring rat folic acid absorption at 21 days postpartum was carried out. The rats were divided into four groups: CP, control pups; GP, pups exposed to ethanol only during gestation; LP, pups exposed to ethanol only during lactation; GLP, pups exposed to ethanol during gestation and lactation. Jejunal and ileal loop transport studies were performed using in vivo perfusion at a flow rate of 3 ml/min for 5 min. Folic acid concentrations of 0.25, 0.5, 1, 1.5 and 2.5 microM: were used. Jejunal and ileal absorption values were determined by the difference between the initial and the final amounts of substrate in the perfusate and expressed as picomoles per square centimeter of intestinal surface every 5 min. The results indicated that ethanol consumption by the dams during gestation and/or lactation led to significant changes in V(max), with no significant changes in apparent K(m). These findings suggest that exposure to ethanol during gestational and suckling periods leads to a general delay in postnatal body weight and that intestinal folate absorption appears to be upregulated in suckling rats, this effect being higher in the LP group.

Response of the exocrine pancreas to the CCK on offspring rats of ethanol dams. Effects of folic acid.

AIMS: The aim of this study was to study the reverse effect of folic acid administered during gestation and lactation to ethanol-treated dams, on cholecystokinin Cholecystokinin (CCK) stimulus-secretion coupling in pancreatic exocrine secretion in offspring rats. METHODS: Animals were randomized into three groups: Control group (C) received water and basic diet during pregnancy and lactation period; ethanol-treated rats (E) received ethanol and basic diet; the ethanol+folic acid group (EF) received folic acid supplement concomitantly with ethanol administration. RESULTS: Body and pancreatic weight was lower in offsprings after ethanol treatment. Folic acid supplementation increased these parameters with respect to ethanol rats. After CCK stimulation, a significant decrease in amylase, lipase and chymotrypsin activities in the duodenal juice were detected in ethanol, this trend was partially corrected with folate supplementation. CONCLUSION: Ethanol exerts its action on exocrine pancreatic secretion by two pathways: 'per se' and diminishing the folic acid content, because a folic acid supplement in rats during pregnancy and lactation periods produces an advantageous effect on amylase, lipase and chymotrypsin secretion in their offspring. Although extrapolation from animal studies may be tenuous, the present findings may explain the use of folic acid in the prevention of ethanol-induced damage by increasing the enzyme levels to adequate physiological concentrations.

Effects of prenatal or postnatal ethanol consumption on zinc intestinal absorption and excretion in rats.

AIMS: The effect of ethanol consumption, either during the pregnancy or lactation period, on the altered metabolism of zinc is not well-defined; consequently, this study was performed to analyze the effect of chronic ethanol exposure on milk consumption, serum, milk, duodenal absorption, fecal and urinary excretion of zinc in dams and offspring during either gestation or lactation in the rat. A complementary study was performed regarding pregnancy outcome. We evaluated testosterone values, the offspring born/litter and several indices such as fertility, viable gestations and the survival index. METHODS: To study the effect of chronic alcoholism during gestation or lactation separately, at birth control newborns were cross-fostered to ethanol dams (ED), and the offspring issued from the ethanol treated mothers were cross-fostered to control dams (CD). Thus, three experimental groups of offspring were formed: (i) control offspring receiving no treatment (CO); (ii) offspring exposed to ethanol only during gestation (GO); and (iii) offspring exposed to ethanol only during lactation (LO). All the results were compared with offspring pair-fed groups (PFO) born of the pair-fed dams (PFD). RESULTS: Duodenal absorption of zinc increased significantly in LO offspring when the substrate concentrations in the perfusion medium were 25, 75, and 150 microM. A higher faecal excretion in GO pups compared with those with LO exposure and control groups (CO and PFO). The urine excretion of zinc was higher for LO offspring with respect to the other three experimental groups (CO, GO, and PFO). CONCLUSIONS: Maternal adaptation resulted in zinc retention, adequate to meet the demands of pup's growth in the face of a lower diet intake. The zinc status in pups is regulated by a higher absorption of zinc and intestinal conservation of endogenous fecal zinc after postnatal ethanol consumption. The increase in urinary zinc excretion could be responsible for decreased serum zinc. However, we found an increase in serum zinc probably due to an increase in the zinc absorption values.