Relationships between variable time, percentage of food restriction and liver histology: which alternative is the best for non-alcoholic fatty liver disease (NAFLD) prevention?

The objective of this study was to analyse the hepatic effects of food restriction in an experimental rabbit model. The study comprised 105 rabbits divided into 6 groups. The two control groups were fed ad libitum (ADL) during the entire experiment (C1 and C2). The experimental groups were restricted between 42-49 days of age, where the rabbits received 50g (R1) or 65g (R2) of food per rabbit per day. Others were restricted between 35-42 days of age, where the rabbits received 50g (R3) or 65g (R4) of food per rabbit per day. For liver analysis, 5 rabbits per group were slaughtered at the ages of 49, 56, 63, 70 days from the R1, R2 groups and at 42, 49, 70 days from the R3, R4 groups. All animals from the C1 and C2 groups developed steatosis with inflammation. Animals from the R1 and R2 groups developed steatosis without inflammation while in the R3 and R4 groups steatosis was not visible. In C1 and C2 groups we observed mostly fatty deposit accumulations while in the R1, R2, R3 and R4 groups, more PAS-positive material accumulations were visible. Liver steatosis correlated with inflammation development and interstitial tissue growth. These results can be used in clinical praxis as signs of NAFLD progression. Early food restriction had intense effects on liver morphology and it seems promising that similar approaches could be applied as preventive treatment for NAFLD development

Genetic parameters for the size of udder cisterns in ewes diagnosed by ultrasonography among breeds: Improved valachian, tsigai, lacaune and their crosses

Udder cistern size in ewes was diagnosed by ultrasonography, using a 3.5MHz linear probe applied laterally from side or ventrally from bottom. The acquired ultrasound images were used to digitally determine the left and right cistern sizes. Both cisterns were scanned approximately 12 hours after the last milking. The area of the left (ALC1; 1933.35 mm2) and right udder cisterns (ARC1; 1970.72 mm2), were determined using from side scans of 378 ewes, obtained at different phases of the lactation cycle), for a total of 1198 measurements. The area of the left (ALC2; 2137.67 mm2) and right udder cisterns (ARC2; 2171.12 mm2) as determined using from bottom scans, from 265 ewes; for a total of 753 measurements. The sums of both cross-sectional areas detected by the method from side (SLRC1) was 3904.07 mm2, and by the method from bottom (SLRC2) was 4308.77 mm2. Primary data were processed using REML methodology and the multiple trait animal model, using the programs REMLF90 and VCE 4.0. In the models, animal was ascribed as a random additive genetic effect and ewe as a permanent effect. Control year (7 or 5 levels), lactation stage (4 levels), breed group (9 levels) and parity (3 levels) were all ascribed as fixed effects. We found higher values of heritability (h2) for the parameters determined by the method from bottom. Heritability coefficients for ALC1 and ALC2 were 0.07 and 0.18 respectively, for ARC1 and ARC2 were 0.17 and 0.2 respectively, and for SLRC1 and SLRC2 were 0.12 and 0.17 respectively. Genetic correlations between ARC1 and ARC1 or ARC2 and ARC2 were high (rg= 0.73 and 0.91). Similarly, the correlations between the size of left and/or right cistern and the total size of both cisterns were high using both ways of scanning (rg= 0.90 to 0.98). In conclusion, measuring the size of the udder cisterns from side is recommended, although measurements from bottom show slightly higher heritability coefficients.La taille de la citerne de lait a été diagnostiquée chez les brebis en utilisant l’échographie et la sonde linéaire de 3,5 MHz de deux façons: La méthode de côté et celle de bas. L’échographie a été faite à partir de chaque scan et ensuite la taille du réservoir à gauche et à droite a été mesurée en utilisant la technique numérique. Les deux citernes ont été scannées environ 12 heures après la dernière traite. L’espace gauche de la citerne (ALC1; 1.933.35 mm2) et celui de droite (ARC1; 1.970.72 mm2), détectés par la méthode de côté, ont été diagnostiqués à plusieurs reprises chez 378 brebis (pendant l’allaitement ainsi qu’entre lactations); un total de 1198 mesures ont été effectuées. L’espace gauche de la citerne (ALC2; 2.137.67 mm2) et de droite (ARC2; 2.171.12 mm2), détectés par la méthode du bas, ont également été diagnostiqués à plusieurs reprises, notamment chez 265 brebis; 753 mesures ont été réalisées au total. La somme des deux zones de section transversale détectées par la méthode de côté (SLRC1) était de 3904.07 mm2, et celle détectée par la méthode de fond (SLRC2) était 4308.77 mm2. Les données primaires ont été traitées en utilisant la méthodologie REML et le modèle animal trait multiple, en utilisant des programmes comme REMLF90 et VCE 4.0. En plus de l’effet génétique additif aléatoire des animaux et l’effet permanent des brebis, les modèles incluent l’année de contrôle comme facteur fixe (7 ou 5 niveaux), un stade de lactation (4 niveaux), un groupe de race (9 niveaux) et la parité (3 niveaux). Nous avons trouvé des valeurs plus élevées de h2 pour les paramètres diagnostiqués par la méthode du bas. Le coefficient d’héritabilité pour ALC1 et ALC2 était de 0.07 et 0.18, respectivement; pour ARC1 et ARC2 de 0.17 et 0.2, resp.; et pour SLRC1 et SLRC2 de 0.12 et 0.17, respectivement. Les corrélations génétiques entre ARC1 et ARC1 ou ARC2 et ARC2 étaient élevées (rg= 0.73 ou 0.910). De même, les corrélations entre la taille de la citerne gauche et/ou droite, et la taille totale des deux citernes étaient élevées avec les deux modes de scan (rg= 0.90 à 0.98). En conclusion, la mesure de la taille des citernes de lait par la méthode de côté est plus recommandée, bien que les mesures avec la méthode du bas montrent des coefficients d’héritabilité légèrement plus élevés

Inflammatory Bowel Disease; Correlations with Celiac Disease

Abstract Inflammatory bowel diseases (IBD) are serious health problems and are connected with increased risk of colitis-associated colorectal carcinoma (CAC). It is the most common cause of death in the patients with Crohn's disease and ulcerative colitis. In this short review, we intend to summarise some aspects of the immunological signalling networks that may be involved in the pathogenesis of CAC patients with the perspectives of treatment of the disease. We also focused on the correlation between celiac disease and IBD

Adverse Effects of Methylglyoxal on Transcriptome and Metabolic Changes in Visceral Adipose Tissue in a Prediabetic Rat Model

Excessive methylglyoxal (MG) production contributes to metabolic and vascular changes by increasing inflammatory processes, disturbing regulatory mechanisms and exacerbating tissue dysfunction. MG accumulation in adipocytes leads to structural and functional changes. We used transcriptome analysis to investigate the effect of MG on metabolic changes in the visceral adipose tissue of hereditary hypetriglyceridaemic rats, a non-obese model of metabolic syndrome. Compared to controls, 4-week intragastric MG administration impaired glucose tolerance (p < 0.05) and increased glycaemia (p < 0.01) and serum levels of MCP-1 and TNFα (p < 0.05), but had no effect on serum adiponectin or leptin. Adipose tissue insulin sensitivity and lipolysis were impaired (p < 0.05) in MG-treated rats. In addition, MG reduced the expression of transcription factor Nrf2 (p < 0.01), which controls antioxidant and lipogenic genes. Increased expression of Mcp-1 and TNFα (p < 0.05) together with activation of the SAPK/JNK signaling pathway can promote chronic inflammation in adipose tissue. Transcriptome network analysis revealed the over-representation of genes involved in insulin signaling (Irs1, Igf2, Ide), lipid metabolism (Nr1d1, Lpin1, Lrpap1) and angiogenesis (Dusp10, Tp53inp1)

Oxidative Damage in Sporadic Colorectal Cancer: Molecular Mapping of Base Excision Repair Glycosylases MUTYH and hOGG1 in Colorectal Cancer Patients

Oxidative stress, oxidative DNA damage and resulting mutations play a role in colorectal carcinogenesis. Impaired equilibrium between DNA damage formation, antioxidant status, and DNA repair capacity is responsible for the accumulation of genetic mutations and genomic instability. The lesion-specific DNA glycosylases, e.g., hOGG1 and MUTYH, initiate the repair of oxidative DNA damage. Hereditary syndromes (MUTYH-associated polyposis, NTHL1-associated tumor syndrome) with germline mutations causing a loss-of-function in base excision repair glycosylases, serve as straight forward evidence on the role of oxidative DNA damage and its repair. Altered or inhibited function of above glycosylases result in an accumulation of oxidative DNA damage and contribute to the adenoma-adenocarcinoma transition. Oxidative DNA damage, unless repaired, often gives rise G:C > T:A mutations in tumor suppressor genes and proto-oncogenes with subsequent occurrence of chromosomal copy-neutral loss of heterozygosity. For instance, G>T transversions in position c.34 of a KRAS gene serves as a pre-screening tool for MUTYH-associated polyposis diagnosis. Since sporadic colorectal cancer represents more complex and heterogenous disease, the situation is more complicated. In the present study we focused on the roles of base excision repair glycosylases (hOGG1, MUTYH) in colorectal cancer patients by investigating tumor and adjacent mucosa tissues. Although we found downregulation of both glycosylases and significantly lower expression of hOGG1 in tumor tissues, accompanied with G>T mutations in KRAS gene, oxidative DNA damage and its repair cannot solely explain the onset of sporadic colorectal cancer. In this respect, other factors (especially microenvironment) per se or in combination with oxidative DNA damage warrant further attention. Base excision repair characteristics determined in colorectal cancer tissues and their association with disease prognosis have been discussed as well