The rapid development of the gastrointestinal tract posthatch has been described; however, little information exists concerning the development of the small intestine in the prehatch period. The present study examined the morphological, cellular, and molecular changes occurring in the small intestine toward the end of the incubation period by examining the expression of intestinal genes that code for brush border digestive enzymes and transporters, their biochemical activities, and the morphological changes in the mucosal layer. The results indicated that during the last 3 d of incubation the weight of the intestine, as a proportion of embryo weight, increased from approximately 1% on d 17 of embryonic age to 3.5% at hatch. At this time the villi could be divided into two main developmental stages, differing in their length and shape, with the larger villi often being pear-shaped and the smaller villi being narrower and having a rocket-like shape. However, on d 19 a further stage of villus development was observed. Activities of maltase, aminopeptidase, sodium-glucose transporter (SGLT)-1, and ATPase began to increase on d 19 and further increased on the day of hatch. The expression of mRNA for these brush-border membrane (BBM) enzymes and transporters was detected from d 15. Determining quantities relative to beta-actin indicated that expression of all parameters examined was low on d 15 and 17, increased 9- to 25-fold on d 19, and all decreased again on the day of hatch. Relative expression of mRNA of the different enzymes and transporters were correlated as were their activities (r = 0.75 to 0.96); however, expression was not correlated with enzymatic activities. The role of these parameters in the ontogeny of absorption is discussed. Thus, major changes in the expression and localization of the functional brush-border proteins prepare the framework for ingestion of carbohydrate- and protein-rich exogenous feed posthatch.

Reproductive failure associated with heat stress is a well-known phenomenon. The mechanism involved in this failure is not clearly understood. In order to test a possible direct effect of heat stress on ovarian function, 36 White Leghorn laying hens were housed in individual cages in 2 temperature- and light-controlled rooms (n = 18). At 31 wk of age, one group was exposed daily for 12 h to high temperature (42 +/- 3 degrees C), and the second group was maintained under thermoneutral conditions (24 to 26 degrees C) and served as control. Body temperature, feed intake, egg production, and egg weight were recorded daily; heparinized blood samples were drawn every 3 d for plasma hormonal level of luteinizing hormone, follicular stimulating hormone, progesterone, 17beta-estradiol, and testosterone. Six days after exposure half of the birds in each group were killed, and the ovary and oviduct were weighed and preovulatory follicles removed and extracted for mRNA of Cytochrome P 450 aromatase, 17-alpha hydroxylase. The same procedure was repeated 9 d later with the rest of the birds. Short and long heat exposure caused significant hyperthermia and reduction of egg production, egg weight, ovarian weight, and the number of large follicles. In addition, a significant reduction in plasma progesterone and testosterone was detected 2 d after exposing the birds to heat stress, and plasma 17beta-estradiol was significantly reduced 14 d after initiation of heat stress. Short exposure to heat stress caused significant reduction in mRNA expression of cytochrome P450 17-alpha hydroxylase, exposing the birds to long-term heat stress caused significant reduction in expression of mRNA of both steroidogenic enzymes. No significant change was found in plasma luteinizing hormone and follicular stimulating hormone levels during the entire experimental period. We suggest a possible direct effect of heat stress on ovarian function.

The influence of photoperiod manipulation in the dry period was examined in dairy goats experiencing environmental heat stress. Multiparous Israeli Saanen goats were blocked at dry off (∼60 d prepartum) into 2 groups of 4 goats each based on body weight, previous milk production, and detected embryo number. Treatments consisted of long-day (16 h light:8 h dark) and short-day (8 h light:16 h dark) photoperiods (LDPP and SDPP, respectively). Heat-stress conditions were applied by manipulating the environment of metabolic rooms to reach a maximum temperature of 37°C between 1000 and 2200 h, and a minimum of 23°C and 70.3% relative humidity. All goats were returned to ambient photoperiod after kidding, milked twice daily, and milk yield was automatically recorded. Dry matter intake during the dry period was similar between treatments, averaging 1,114 g/d. Milk production was significantly higher in the SDPP than the LDPP group (2,172 vs. 1,550 g/d) during the 12-wk experimental period. Milk protein and fat contents were similar in both groups and averaged 3.63 and 4.34%, respectively, whereas milk lactose was higher in the LDPP group (4.77 vs. 4.67%). Heart rates were similar between treatments and averaged 112.6 beats per minute (BPM). Respiration rates were lower in the morning (58.4 BPM) compared with the afternoon (91.2 BPM) and were not influenced by photoperiod. Rectal temperature was higher for the LDPP than the SDPP group (40.4 vs. 39.6°C). The thyroid hormone level (mean ± SE) was similar in both groups during the dry period, but higher during lactation in the LDPP goats up to 40 d postpartum (110±6.59 vs. 156±8.76 ng/mL). Plasma IGF-1 (mean ± SE) was higher in the LDPP group (279±62 vs. 162±27 ng/mL in SDPP) during the dry period but was similar postkidding, averaging 132±24 ng/mL. Plasma prolactin level (mean ± SE) was higher in the LDPP than the SDPP group during the dry period (17.2±1.6 vs. 10.6±0.99 ng/mL), whereas it was similar throughout lactation (0.61±0.28 ng/mL). These data support the idea that SDPP manipulation during heat load in dry goats can be used as an abatement strategy to reduce the carryover effect of heat stress observed during the subsequent lactation. The higher milk production in SDPP goats is explained by changes in circulating prolactin profile rather than differences in feed intake or secretion of insulin-like growth factor 1.

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.

1. The effect of vitamin A on the small intestine was examined in vitamin-A-deficient meat-type chickens. 2. Maturation and activity of the small intestinal cells were assayed by detection of proliferating cells with proliferating cells nuclear antigen, goblet cells with Alcian blue, mature cells with alkaline phosphatase and extent of RNA expression with dot blot analysis. 3. Vitamin A deficiency caused hyperproliferation of enterocytes, a decrease in the number of goblet cells, decreased alkaline phosphatase activity and decreased expression of 2 brush-border enzymes. 4. Our findings suggest that the absence of vitamin A interferes with the normal growth rate in chickens because it influences functionality of the small intestine by altering proliferation and maturation of cells in the small intestinal mucosa.