Biomedical subjects

A Geyra

Publications and source records attributed to A Geyra.

8 recordsLinked to original sources

PubMed2003

The effect of chronic feeding of diacetoxyscirpenol and T-2 toxin on performance, health, small intestinal physiology and antibody production in turkey poults.

1. The effects of feeding T-2 toxin or diacetoxyscirpenol (DAS) at levels up to 1 ppm for 32 d on performance, health, small intestinal physiology and immune response to enteral and parenteral immunisation were examined in young poults. 2. Slight improvement in growth was observed in some groups of poults fed T-2 or DAS mycotoxins for 32 d, with no change in feed efficiency. Feeding both T-2 and DAS resulted in oral lesions which had maximal severity after 7-15 d. 3. Mild intestinal changes were observed at 32 d but no pathological or histopathological lesions were found. Both mycotoxins altered small intestinal morphology, especially in the jejunum where villi were shorter and thinner. In addition, both DAS and T-2 mycotoxins enhanced the proportion of proliferating cells both in the crypts and along the villi. Migration rates were reduced in the jejunum of poults fed T-2 toxin but did not change in the duodenum or in poults fed DAS. 4. No significant effects of T-2 or DAS were observed on antibody production to antigens administered by enteral or parenteral routes. 5. This study indicates that tricothecene toxins at concentrations of up to 1 ppm for more than 30 d influenced small intestinal morphology but did not affect growth or antibody production.

Administration, Oral↗

PubMed2002

Starving affects CDX gene expression during small intestinal development in the chick.

The small intestine of the chicken undergoes intensive changes in the immediate posthatch period, increasing in size and developing crypts, villi and mature enterocytes. During this time, chicks are also transferring from nutrition based on the lipid-rich yolk to exogenous carbohydrate-rich feeds. The cdx homeobox genes participate in axial patterning and in definition of cell identity in embryos, and some cdx genes remain active postpartum in organs such as the intestine. In this study, the transcription patterns of two of these genes, cdxA and cdxB, were examined in the small intestine of the embryo and posthatch chick; in addition, the effects on these genes of starving for 48 h at hatch were examined. Both cdx transcription factors were upregulated toward the time of hatch and were observed in proliferating enterocytes; this enhanced expression continued posthatch. Distribution of cdxA changed with age and was found at higher concentrations in mature enterocytes. Starving from 0 to 48 h posthatch retarded growth and decreased enterocyte proliferation and expression of cdxA and cdxB. After access to feed, expression of cdx genes was enhanced. Chicken homeobox genes cdxA and cdxB are expressed in all enterocytes during embryonic and posthatch development; however, cdxA may have a role in enterocyte maturation posthatch. CdxB was expressed later in development then previously reported.

Animals↗

PubMed2001

The effect of fasting at different ages on growth and tissue dynamics in the small intestine of the young chick.

The small intestines of hatching chicks undergo rapid developmental changes in the immediate post-hatch period when the birds are making the transition from endogenous nutrient supply from yolk to dependence on exogenous feed. This transition usually only begins 48 h or more after hatching, owing to logistical considerations of production. The effects of fasting for 48 h at different times during this critical period on small intestinal development and enterocyte dynamics were examined by morphometric determinations and use of staining for proliferative-cell nuclear antigen and 5-bromo-2-deoxyuridine. The effects of fasting were specific to both time of fasting and the intestinal segment examined. Decreased development was found in the duodenum and jejunum, but was less apparent in the ileum. Fasting between 0 and 48 h decreased crypt size in the duodenum and jejunum, the number of crypts per villus, crypt proliferation, villus area and the rate of enterocyte migration. Fasting at later times resulted in smaller effects, although the jejunum appeared to be the most sensitive of the intestinal segments. Growth was correlated with the number of cells in the crypts, the number of cells along the villus and the segment surface area. The common practice whereby feed is first available to chicks more than 48 h post-hatch may depress subsequent development.

Animals↗

PubMed2001

Changes in growth and function of chick small intestine epithelium due to early thermal conditioning.

The effect of exposure to heat at 3 d of age on small intestine functionality and development was assayed by measuring villus size, proliferating enterocytes, and brush-border membrane (BBM) enzyme expression and activity. Results showed that thermal conditioning caused an immediate effect characterized by lowered triiodothyronine (T3) level, reduced feed intake, and depressed enterocyte proliferation and BBM enzyme activity. A second series of effects, observed 48 h posttreatment, was characterized by elevated T3, increased feed intake, increased enterocyte proliferation, and higher expression and activity of BBM enzymes. The association between ambient temperature, feed intake, growth rate, and plasma T3 levels was reflected in the structure and function of the intestinal tract. The results suggest that thermal conditioning at an early age influences T3 concentrations, which in turn alter the intestinal capacity to proliferate, grow, and digest nutrients. However, these experiments were not able to discriminate between effects due to feed intake and those due to thermal conditioning. The treatments modulated changes in the intestinal tract following thermal treatment.

Adaptation, Physiological↗

PubMed2001

Enterocyte dynamics and mucosal development in the posthatch chick.

Changes in the morphology of the small intestinal mucosa and enterocyte dynamics were examined in posthatch chicks through 12 d. At hatch, enterocytes were round and nonpolar; however, within 24 h posthatch, enterocytes lengthened and exhibited more typical morphology. Crypts were rudimentary at hatch and by 48 h invagination was completed and crypt numbers increased by branching and fission, with the number of crypts per villus reaching plateau after 72 h posthatch. All epithelial cells were proliferative at hatch. In the crypts, the proportion of proliferating enterocytes decreased to 50 to 60% within 2 d posthatch, whereas along the villus the proportion of proliferating cells decreased to 10 to 20% by 6 d. Different patterns of temporal development of villi were observed in the duodenum, jejunum and ileum. Individual villus surface area increased steadily in the duodenum throughout the experiment, whereas individual jejunal and ileal villus surface areas increased more slowly after 4 d posthatch. The number of villi per cross-section of intestine increased in the duodenum and jejunum but not in the ileum. The total segment villus surface area increased similarly in all segments until 3 d posthatch, after which the jejunum increased considerably in absorptive area, whereas the duodenum and ileum increased more slowly. This study shows that, in the hatching chick, the small intestine matures in a manner similar to neonatal mammals, with specific ontogenetic timetables in the different small intestinal segments, however, the most dramatic changes occur within the first 24 h posthatch.

Animals↗

PubMed2001

The effect of early feeding on growth and small intestinal development in the posthatch poult.

Poults with early access to feed in the hatchery or turkey house grew more than those reared under standard commercial practice. During 48 h posthatch, fed poults utilized yolk and exogenous feed to increase BW by 11 g. The small intestine increased from 3.8% of BW at hatch to 8.9% after 48 h. In contrast, BW in feed-deprived poults decreased by 10 g, whereas the small intestine increased slightly in weight and composed 4.5% of BW after 48 h. The number of cells per villus and the villus surface area increased dramatically posthatch in the duodenum but more slowly in the jejunum and ileum. Enterocyte width changed little, but length increased more than twofold in the duodenum and by approximately 50% in the jejunum and ileum by 6 d posthatch. Lack of access to feed depressed the rate of growth of villi and enterocyte length in all intestinal segments until 6 d posthatch. All intestinal epithelial cells were proliferating at hatch, which changed rapidly within 48 h posthatch, with proliferating cells becoming located mainly in the intestinal crypts where about half of the cells were proliferating. In feed-deprived poults, the decrease in the proportion of proliferating cells in the crypt was greater than that of fed poults; after refeeding, an increase in the rate of proliferation was observed in feed-deprived poults. Plasma concentrations of Na, glucose, triglycerides, and phospholipids were not affected by feed deprivation; however, nonesterified fatty acid concentrations were enhanced in feed-deprived poults, indicating a greater use of fatty acids for energy. Plasma triiodothyronine (T3) concentrations, which may mediate some of the intestinal effects of feed deprivation, were depressed in poults without access to feed.

Aging↗

PubMed2000

Small intestinal development in the young chick: crypt formation and enterocyte proliferation and migration.

1. Post-natch mucosal development was examined in the chick small intestinal epithelium using immunostaining with proliferating cell nuclear antigen (PCNA) and 5-bromo-2-deoxyuridine (BrdU). 2. On the day of hatching jejunal crypts were small and a single crypt per villus was observed. However, during the 108 h post-hatch crypts developed rapidly branching and increasing in size, cell numbers and cell size. 3. Almost all epithelial cells in the small intestine of the hatching chick were proliferating, as indicated by PCNA and BrdU, while more than 80% of proliferating cells were localised in the crypts after 108 h post hatch. 4. Estimate of villus cell transit time using BrdU was only possible from 48 h post-hatch when villus transit time was 72 h in the jejunum, whereas at 336 h transit time was 96 h. 5. In the 108 h post hatch a rapid transition occurs from total jejunal epithelial cell proliferation and immature crypts to a defined proliferative zone in the crypts, with constant division and migration.

Animals↗

PubMed2000

Early posthatch starvation decreases satellite cell proliferation and skeletal muscle growth in chicks.

The effect of posthatch starvation on skeletal muscle growth and satellite cell proliferation was examined in chicks. Chicks were either fed or starved for 48 h posthatch (d 0-d 2, d 2-d 4 or d 4-d 6) and then refed for 41 d. Body and breast muscle weights were significantly lower in starved chicks than in fed controls throughout the experiment. Histochemical staining revealed that skeletal muscle fiber development in the starved group lagged behind that of the fed group. Starvation from d 2 to 4 and d 4 to 6 posthatch had a progressively lesser effect than did immediate posthatch starvation (P < 0.05). In vitro culturing of breast muscle satellite cells revealed that DNA synthesis and number of cells per gram of muscle in the fed chicks peaked on d 2 and d 3, and then declined. In contrast, DNA synthesis in the cells of starved chicks declined on d 2 and increased on d 3 when chicks were refed. A similar pattern was seen for the number of cells per gram muscle; however, in general cell numbers tended to be higher in the starved group than in controls (P < 0.1). The results obtained with cultured cells were parallel with in situ immunostaining with 5-bromo-2'-deoxyuridine and proliferating cell nuclear antigen in breast muscle from experimental chicks, and with growth hormone receptor expression. These results suggest that satellite cell cultures are a reliable tool for evaluating muscle growth in postnatal chickens. We conclude that sufficient feed in the immediate postnatal period is critical for satellite cell proliferation and skeletal muscle development and is thus important for optimal muscle growth.

Aging↗