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.

Isocaloric high-fat feeding directs hepatic metabolism to handling of nutrient imbalance promoting liver fat deposition.

BACKGROUND/OBJECTIVES: Consumption of fat-rich foods is associated with obesity and related alterations. However, there is a group of individuals, the metabolically obese normal-weight (MONW) subjects, who present normal body weight but have metabolic features characteristic of the obese status, including fat deposition in critical tissues such as liver, recognized as a major cause for the promotion of metabolic diseases. Our aim was to better understand metabolic alterations present in liver of MONW rats applying whole genome transcriptome analysis. METHODS: Wistar rats were chronically fed a high-fat diet isocaloric relative to Control animals to avoid the hyperphagia and overweight and to mimic MONW features. Liver transcriptome analysis of both groups was performed. RESULTS: Sustained intake of an isocaloric high-fat diet had a deep impact on the liver transcriptome, mainly affecting lipid metabolism. Although serum cholesterol levels were not affected, circulating triacylglycerols were lower, and metabolic adaptations at gene expression level indicated adaptation toward handling the increased fat content of the diet, an increased triacylglycerol and cholesterol deposition in liver of MONW rats was observed. Moreover, gene expression pointed to increased risk of liver injury. One of the top upregulated genes in this tissue was Krt23, a marker of hepatic disease in humans that was also increased at the protein level. CONCLUSION: Long-term intake of a high-fat diet, even in the absence of overweight/obesity or increase in classical blood risk biomarkers, promotes a molecular environment leading to hepatic lipid accumulation and increasing the risk of suffering from hepatic 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.

The intake of high-fat diets induces the acquisition of brown adipocyte gene expression features in white adipose tissue.

BACKGROUND/OBJECTIVE: White-to-brown adipose tissue remodeling (browning) in response to different stimuli constitutes an active research area for obesity treatment. The emergence in traditional white adipose tissue (WAT) depots of multilocular adipocytes that express uncoupling protein 1 (UCP1) and resemble brown adipocytes, the so called 'brite' adipocytes, could contribute to increased energy expenditure. In rodents, obesogenic stimuli such as the intake of hyperlipidic diets can increase brown adipose tissue (BAT) thermogenic capacity and contribute to maintaining body weight. The aim of this study was to investigate the potential of two different hyperlipidic diets, a commercial high-fat (HF) diet and a highly palatable cafeteria (CAF) diet, to induce WAT browning. METHODS: We analyzed gene expression of a wide number of brown/brite adipocyte markers in different WAT depots, in BAT and in peripheral blood mononuclear cells (PBMCs) increasingly being used in nutrition studies as a potential source of biomarkers of physiological effects. We also performed morphological analysis of adipose tissue. RESULTS: Both HF diets studied were able to increase the expression of the markers studied in WAT in a depot-specific manner, as well as in BAT; some of these changes were also reflected in PBMCs. This increased browning capacity was translated into the appearance of UCP1- and CIDE-A (cell death-inducing DFFA-like effector A)-positive brite adipocytes in retroperitoneal WAT. Administration of the CAF diet, associated with higher adiposity, produced the strongest impact on the parameters studied while its withdrawal restored basal conditions. CONCLUSIONS: Acquisition of brown adipocyte features in WAT could evidence an adaptation to try to counteract increased adiposity due to the intake of HF diets. Additionally, PBMCs could constitute an interesting easily obtainable material to assess the effect of nutritional interventions on browning capacity.

Diet-induced obesity affects expression of adiponutrin/PNPLA3 and adipose triglyceride lipase, two members of the same family.

BACKGROUND: Adiponutrin/PNPLA3 and adipose triglyceride lipase (ATGL) are proteins highly expressed in adipose tissue which have apparently different roles (lipogenic/lipolytic). Gene expression of both proteins and their nutritional regulation have been described to be altered in genetically obese animals. METHODS: We studied adiponutrin and ATGL expression in 6-month-old rats made obese by cafeteria diet feeding, submitted to different feeding conditions (feeding/fasting/re-feeding), compared with normoweight animals. Adiponutrin and ATGL mRNA levels were determined in white adipose tissue depots (subcutaneous and visceral) and in interscapular brown adipose tissue, and ATGL protein levels in selected depots. In addition, basal adiponutrin and ATGL expression levels were compared between 6- and 3-month-old animals. RESULTS: Obesity decreased adiponutrin and ATGL expression in different adipose depots. For adiponutrin, a tendency to lower mRNA levels was observed in the white adipose depots studied in obese animals, although the decrease was only significant in the subcutaneous depot. For ATGL, a generalized and significant lower expression was found in white and brown adipose tissue of cafeteria-obese rats. When considering nutritional regulation, according to a lipogenic role, adiponutrin mRNA expression decreased with fasting and was recovered by re-feeding in normoweight animals; this regulation was lost in obese rats. Expression of the lipolytic ATGL (mRNA and protein levels) was increased by fasting in normoweight animals in the mesenteric adipose depot, while no change was evident in obese rats. Moreover, adiponutrin and ATGL nutritional regulation was affected by age, and we report a downregulation of adiponutrin mRNA basal levels with age in internal adipose depots. CONCLUSIONS: Cafeteria diet-induced obesity and age alter adiponutrin and ATGL expression and their regulation by feeding conditions. These results reinforce the importance of a proper expression and regulation of both proteins for body weight maintenance and their role in energy metabolism.

The interferon-gamma field trial: background, principles and progress.

Since November 2002, the State Veterinary Service and the Veterinary Laboratories Agency have been conducting a field trial to assess the interferon-gamma test as an ancillary parallel test to the tuberculin skin test in herds with confirmed tuberculosis breakdowns. Here, Martin Vordermeier, Tony Goodchild, Richard Clifton-Hadley and Ricardo de la Rua describe the background to the trial, discuss the principle of the test and provide an update of progress so far

The clinical and histological spectrum of esophagitis in pediatrics. Some keys to its links to gastritis.

UNLABELLED: The purpose of our study was to assess the clinical and histological spectrum of esophagitis, seeking possible links between esophagitis and gastritis particularly Helicobacter pylori-associated, in pediatric patients. MATERIAL AND METHODS: We retrospectively studied 66 sequential and 63 gastric biopsies from 66 patients fulfilling the histological diagnosis of "esophagitis". Cases were arranged in two groups: G1 (H. pylori negative): N = 44 (27 m; 17 f), mean age 7.3 y (range 7-9 m-18 y) and G2 (H. pylori positive): N = 22 (16 f; 6 m), mean age 12.8 y (range 7-16 y). RESULTS: The bases for performing endoscopy and biopsies were as follows: in G1 (N44) symptoms of gastroesophageal reflux (GER) in 24 cases and non-GER in 20 cases; in G2 (N = 22): symptoms of GER in 13 and non-GER in 9 cases. Esophageal endoscopic findings for G1 patients included: normal mucosa 39; esophagitis 3; congestive mucosa and esophagitis 1 each. Stomach endoscopic findings for G1 patients were normal mucosa 29; nodular antrum 7; congestive mucosa 4; ulceration 2; unknown 2. G2 children revealed nodular antrum 19; congestive antrum 2; normal mucosa 1. Histology of esophageal biopsies in G1 was esophagitis grade 1,35; grade 2,4; grade 3, 4, and grade 5, 1. G2 showed esophagitis grade 1,20, and grade 2,2. The histologic findings of the gastric biopsies were as follows: G1 (N = 41): normal mucosa 23; mild chronic gastritis 6; mucus depletion in the superficial 5; mild acute gastritis 3; hemorrhage 1; insufficient tissue 3. G2: chronic gastritis associated with H. pylori with or without follicular hyperplasia 21; mild gastritis 1.

The clinical and histological spectrum of esophagitis in pediatrics. Some keys to its links to gastritis

The purpose of our study was to assess the clinical and histological spectrum of esophagitis, seeking possible links between esophagitis and gastritis particularly Helicobacter pylori-associated, in pediatric patients. MATERIAL AND METHODS: We retrospectively studied 66 sequential and 63 gastric biopsies from 66 patients fulfilling the histological diagnosis of "esophagitis". Cases were arranged in two groups: G1 (H. pylori negative): N = 44 (27 m; 17 f), mean age 7.3 y (range 7-9 m-18 y) and G2 (H. pylori positive): N = 22 (16 f; 6 m), mean age 12.8 y (range 7-16 y). RESULTS: The bases for performing endoscopy and biopsies were as follows: in G1 (N44) symptoms of gastroesophageal reflux (GER) in 24 cases and non-GER in 20 cases; in G2 (N = 22): symptoms of GER in 13 and non-GER in 9 cases. Esophageal endoscopic findings for G1 patients included: normal mucosa 39; esophagitis 3; congestive mucosa and esophagitis 1 each. Stomach endoscopic findings for G1 patients were normal mucosa 29; nodular antrum 7; congestive mucosa 4; ulceration 2; unknown 2. G2 children revealed nodular antrum 19; congestive antrum 2; normal mucosa 1. Histology of esophageal biopsies in G1 was esophagitis grade 1,35; grade 2,4; grade 3, 4, and grade 5, 1. G2 showed esophagitis grade 1,20, and grade 2,2. The histologic findings of the gastric biopsies were as follows: G1 (N = 41): normal mucosa 23; mild chronic gastritis 6; mucus depletion in the superficial 5; mild acute gastritis 3; hemorrhage 1; insufficient tissue 3. G2: chronic gastritis associated with H. pylori with or without follicular hyperplasia 21; mild gastritis 1.

The clinical and histological spectrum of esophagitis in pediatrics. Some keys to its links to gastritis

The purpose of our study was to assess the clinical and histological spectrum of esophagitis, seeking possible links between esophagitis and gastritis particularly Helicobacter pylori-associated, in pediatric patients. MATERIAL AND METHODS: We retrospectively studied 66 sequential and 63 gastric biopsies from 66 patients fulfilling the histological diagnosis of "esophagitis". Cases were arranged in two groups: G1 (H. pylori negative): N = 44 (27 m; 17 f), mean age 7.3 y (range 7-9 m-18 y) and G2 (H. pylori positive): N = 22 (16 f; 6 m), mean age 12.8 y (range 7-16 y). RESULTS: The bases for performing endoscopy and biopsies were as follows: in G1 (N44) symptoms of gastroesophageal reflux (GER) in 24 cases and non-GER in 20 cases; in G2 (N = 22): symptoms of GER in 13 and non-GER in 9 cases. Esophageal endoscopic findings for G1 patients included: normal mucosa 39; esophagitis 3; congestive mucosa and esophagitis 1 each. Stomach endoscopic findings for G1 patients were normal mucosa 29; nodular antrum 7; congestive mucosa 4; ulceration 2; unknown 2. G2 children revealed nodular antrum 19; congestive antrum 2; normal mucosa 1. Histology of esophageal biopsies in G1 was esophagitis grade 1,35; grade 2,4; grade 3, 4, and grade 5, 1. G2 showed esophagitis grade 1,20, and grade 2,2. The histologic findings of the gastric biopsies were as follows: G1 (N = 41): normal mucosa 23; mild chronic gastritis 6; mucus depletion in the superficial 5; mild acute gastritis 3; hemorrhage 1; insufficient tissue 3. G2: chronic gastritis associated with H. pylori with or without follicular hyperplasia 21; mild gastritis 1. (AU)

The clinical and histological spectrum of esophagitis in pediatrics. Some keys to its links to gastritis.

The purpose of our study was to assess the clinical and histological spectrum of esophagitis, seeking possible links between esophagitis and gastritis particularly Helicobacter pylori-associated, in pediatric patients. MATERIAL AND METHODS: We retrospectively studied 66 sequential and 63 gastric biopsies from 66 patients fulfilling the histological diagnosis of [quot ]esophagitis[quot ]. Cases were arranged in two groups: G1 (H. pylori negative): N = 44 (27 m; 17 f), mean age 7.3 y (range 7-9 m-18 y) and G2 (H. pylori positive): N = 22 (16 f; 6 m), mean age 12.8 y (range 7-16 y). RESULTS: The bases for performing endoscopy and biopsies were as follows: in G1 (N44) symptoms of gastroesophageal reflux (GER) in 24 cases and non-GER in 20 cases; in G2 (N = 22): symptoms of GER in 13 and non-GER in 9 cases. Esophageal endoscopic findings for G1 patients included: normal mucosa 39; esophagitis 3; congestive mucosa and esophagitis 1 each. Stomach endoscopic findings for G1 patients were normal mucosa 29; nodular antrum 7; congestive mucosa 4; ulceration 2; unknown 2. G2 children revealed nodular antrum 19; congestive antrum 2; normal mucosa 1. Histology of esophageal biopsies in G1 was esophagitis grade 1,35; grade 2,4; grade 3, 4, and grade 5, 1. G2 showed esophagitis grade 1,20, and grade 2,2. The histologic findings of the gastric biopsies were as follows: G1 (N = 41): normal mucosa 23; mild chronic gastritis 6; mucus depletion in the superficial 5; mild acute gastritis 3; hemorrhage 1; insufficient tissue 3. G2: chronic gastritis associated with H. pylori with or without follicular hyperplasia 21; mild gastritis 1.