Search

Copyright of Agro Productividad is the property of Colegio de Postgraduados and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Agro Productividad is the property of Colegio de Postgraduados and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Hypothyroidism is associated with the development of non-alcoholic steatohepatitis, but cellular mechanisms have been scarcely analyzed. Thyroid hormones regulate the synthesis and secretion of bile acids that are endogenous ligands of the farnesoid receptor (FXRa), which have been involved in the development of non-alcoholic steatohepatitis. However, the relationship between thyroid hormones and FXRa expression in the liver is yet unknown. Control (n = 6) and methimazole-induced hypothyroid (n = 6) female rabbits were used to evaluate the amount of lipids and glycogen, vascularization, hepatocytes proliferation, immune cells infiltration, and expression of FXRa. Student-t or Mann-Whitney U tests were carried out to determine significant differences. Hypothyroidism induced steatosis, glycogen loss, fibrosis, and a minor vascularization in the liver. In contrast, hypothyroidism increased the proliferation of hepatocytes and the infiltration of mast cells, but did not modify the number of immune cells into sinusoids. These changes were associated with a minor anti-FXRa immunoreactivity of periportal hepatocytes and pericentral immune cells. Our results suggest that hypothyroidism induces a moderate non-alcoholic steatohepatitis, alllowing the hepatic regeneration. The FXRa may be involved in the development of non-alcoholic steatohepatitis in hypothyroid subjects. [ABSTRACT FROM AUTHOR]

Contents Oviductal regions show particular histological characteristics and functions. Tubal pathologies and hypothyroidism are related to primary and secondary infertility. The impact of hypothyroidism on the histological characteristics of oviductal regions has been scarcely studied. Our aim was to analyse the histological characteristics of oviductal regions in control and hypothyroid rabbits. Hypothyroidism was induced by oral administration of methimazole ( MMI) for 30 days. For both groups, serum concentrations of thyroid and gonadal hormones were determined. Sections of oviductal regions were stained with the Masson's trichrome technique to analyse both epithelial and smooth muscle layers. The percentage of proliferative epithelial cells (anti-Ki67) in diverse oviductal regions was also quantified. Data were compared with Student t-test, Mann-Whitney U-test, or Fischer's test. In comparison with the control group, the hypothyroid group showed: (i) a low concentration of T3 and T4, but a high level of TSH; (ii) similar values of serum estradiol, progesterone and testosterone; (iii) a large size of ciliated cells in the ampulla ( AMP), isthmus ( IST) and utero-tubal junction ( UTJ); (iv) a large size of secretory cells in the IST region; (v) a low percentage of proliferative secretory cells in the fimbria-infundibulum ( FIM- INF) region; and (vi) a similar thickness of the smooth muscle layer and the cross-sectional area in the AMP and IST regions. Modifications in the size of the oviductal epithelium in hypothyroid rabbits could be related to changes in the cell metabolism that may impact on the reproductive functions achieved by oviduct. [ABSTRACT FROM AUTHOR]

Objectives A growing incidence of pediatric IBD (PIBD) in southern Europe has been recently reported. The SPIRIT registry (1996-2009) confirmed these tendencies in Spain. Our aim is to obtain data from 1985 to 1995 and describe the complete picture of PIBD presentation changes in Spain in the last 25 years. Methods A retrospective survey of incident PIBD in the period 1985-1995 was performed. Patients' data were obtained from the hospitals' databases and compared with the published data from the 1996 to 2009 period. Seventy-eight IBD reference centers took part in this survey. Results Data from 495 patients were obtained: 278 CD (56.2%), 198 UC (40%), and 19 IBDU (3.8%); 51.7% were female, with higher predominance both in UC (58.6%) and in IBDU (57.9%), but not in CD (46.4%). Median (IQR) age at diagnosis was 12.9 (10.0-15.7) years, with significant differences among IBD subtypes: CD: 13.1 (10.8-16.0) vs UC: 12.4 (9.4-15.1) vs IBDU: 7.5 (3.0-13.0) (p ≤ 0.001). These results are significantly different to the ones in the SPIRIT registry, with a higher proportion of IBDU, younger age and male predominance. The data from both periods taken together give a complete picture of a 25--year period. An annual increase of incident patients was observed, with a ten-fold increase over this period. Conclusion These data extend the epidemiological trends to a full 25--year period (1985-2009). PIBD incidence in Spain has experienced a sixteen-fold increase. The IBD subtype, localization of the affected segment, age- and sex distribution observed are in accordance with our previously published ones of 1996-2009. [ABSTRACT FROM AUTHOR]

Poor maternal nutrition predisposes offspring to metabolic disease. This predisposition is modified by various postnatal factors. We hypothesised that coupled to the initial effects of developmental programming due to a maternal low-protein diet, a second hit resulting from increased offspring postnatal sugar consumption would lead to additional changes in metabolism and adipose tissue function. The objective of the present study was to determine the effects of sugared water consumption (5 % sucrose in the drinking-water) on adult offspring adiposity as a ‘second hit’ following exposure to maternal protein restriction during pregnancy. We studied four offspring groups: (1) offspring of mothers fed the control diet (C); (2) offspring of mothers fed the restricted protein diet (R); (3) offspring of control mothers that drank sugared water (C-S); (4) offspring of restricted mothers that drank sugared water (R-S). Maternal diet in pregnancy was considered the first factor and sugared water consumption as the second factor – the second hit. Body weight and total energy consumption, before and after sugared water consumption, were similar in all the groups. Sugared water consumption increased TAG, insulin and cholesterol concentrations in both the sexes of the C-S and R-S offspring. Sugared water consumption increased leptin concentrations in the R-S females and males but not in the R offspring. There was also an interaction between sugared water and maternal diet in males. Sugared water consumption increased adipocyte size and adiposity index in both females and males, but the interaction with maternal diet was observed only in females. Adiposity index and plasma leptin concentrations were positively correlated in both the sexes. The present study shows that a second hit during adulthood can amplify the effects of higher adiposity arising due to poor maternal pregnancy diet in an offspring sex dependent fashion. [ABSTRACT FROM PUBLISHER]