Glucagon-like peptide 2 therapy reduces negative effects of diarrhea on calf gut.

Damage to the intestinal epithelium reduces nutrient absorption and animal growth, and can have negative long-term health effects on livestock. Because the intestinotropic hormone glucagon-like peptide 2 (GLP-2) has been shown to contribute to gut integrity, reduce inflammation, and improve nutrient absorption, the present study was designed to determine whether administration of GLP-2 to calves with coccidiosis in the first month of life affects intestinal growth and mediates negative effects of the proinflammatory response. Holstein bull calves (n=19) were assigned to 4 treatment groups of 4 to 5 calves each: (1) infected with Eimeria bovis, GLP-2 treated; (2) noninfected, GLP-2 treated; (3) infected with E. bovis, buffer treated; and (4) noninfected, buffer treated. Infected calves received 100,000 to 200,000 sporulated E. bovis oocysts suspended in milk replacer on d 0 of the study. On d 18, calves in the GLP-2 groups received a subcutaneous injection of 50 µg of bovine GLP-2/kg of body weight twice daily for 10 d, and calves in the buffer-treated groups received an equivalent volume of sodium bicarbonate buffer only. On d 28, calves were slaughtered 2h after injection of 5-bromo-2'-deoxyuridine (BrdU). Intestinal tissues were measured and villus height, crypt depth, and BrdU immunostaining were evaluated in segments of the small intestine. Nitrotyrosine immunostaining, a measure of nitro-oxidative damage, was evaluated in the ileum and cecum. No GLP-2 treatment by E. bovis infection interaction was observed for any parameter measured, with the exception of nitrotyrosine immunostaining in the cecum. Large intestinal weight was greater in infected than noninfected calves and with GLP-2 treatment relative to buffer treatment. Calves that received GLP-2 also had greater small intestinal weight but no difference in cell proliferation, as assessed by BrdU labeling, relative to buffer-treated calves. No treatment effects were detected for villus height, crypt depth, or villus height:crypt depth ratio in segments of the small intestine. Protein tyrosine nitration was over 3-fold greater in the ileum and cecum of infected calves relative to noninfected calves, and GLP-2 therapy reduced tyrosine nitration in infected calves by 47% in the ileum and 69% in the cecum relative to buffer-treated calves. Treatment with GLP-2 promotes intestinal growth in neonatal calves and reduces the detrimental effects of nitro-oxidative stress in the ileocecum of calves with coccidiosis.

The effect of intrauterine growth retardation on the expression of developmental factors in porcine placenta subsequent to the initiation of placentation.

Intrauterine growth retardation (IUGR) hinders fetal growth and postnatal development in swine; however the etiology of IUGR is essentially unknown. Expression of fourteen candidate genes associated with placental development or IUGR was examined in gestational day 50 (gd50) control and IUGR fetus whole placental tissue or areolae by real-time PCR. Endothelial nitric oxide synthase (ENOS) mRNA expression was elevated in gd50 IUGR placenta and areola compared to gd50 control. Since ENOS could modulate vascular tone and angiogenesis via nitric oxide production, data suggest that the increase in IUGR may be an adaptive response to poor perfusion to maintain pregnancy.

Oxytocin stimulates secretion of prostaglandin F(2alpha) from endometrial cells of swine in the presence of progesterone.

Oxytocin (OT) stimulates endometrial secretion of prostaglandin (PG) F(2 alpha) during corpus luteum regression in swine but there is differential responsiveness to OT among endometrial cell types. To determine if progesterone influenced responsiveness of luminal epithelial, glandular epithelial, and stromal cells to 100 nM OT during luteolysis in swine, cells were isolated from endometrium of 15 gilts by differential enzymatic digestion and sieve filtration on day 16 postestrus and cultured continuously in the presence of 0, 10 or 100 nM progesterone. For phospholipase C (PLC) activity and PGF(2 alpha) secretion, stromal cells were most responsive to OT (P<0.01) in the absence of progesterone, whereas luminal epithelial cells were unresponsive and glandular epithelial cells displayed an intermediate response to OT (P<0.09). Progesterone enhanced PLC activity linearly in glandular epithelial cells (P<0.05) and influenced it quadratically in stromal cells (P=0.05). The effect of OT and progesterone on PLC activity in luminal epithelial cells was not significant, and progesterone did not increase PLC activity in response to OT in any cell type. Culture in the presence of progesterone, enhanced PGF(2 alpha) secretion in response to OT in luminal epithelial cells (P<0.05) but not in glandular epithelial or stromal cells. Progesterone also increased overall PGF(2 alpha) release from glandular epithelial (P<0.05) and stromal cells (P<0.06) across both levels of OT treatment. These results indicate that progesterone enhanced PGF(2 alpha) secretion from luminal epithelial cells in response to OT and increased basal PGF(2 alpha) release from glandular epithelial and stromal cells.

Interestrous interval of cyclic gilts is decreased by systemic but not intrauterine administration of exogenous oxytocin.

Oxytocin (OT) stimulates pulsatile secretion of uterine prostaglandinF2alpha in ruminants, but the role of OT in the estrous cycle regulation of pigs is not clear. These studies were performed to determine the effect of exogenous OT on interestrous interval of intact cyclic gilts. Intrauterine infusion of 80 USP units three times daily on d 10 to 16 after estrus did not decrease interestrous interval (24.5+/-1.3 d) compared with control gilts (22.5+/-1.3 d). In contrast, i.m. injections of 20 USP units of OT twice daily or 80 USP units of OT three times daily on d 10 to 16 after estrus decreased (P < 0.05) interestrous interval (20.0+/-0.3 or 19.5+/-0.4 d, respectively) compared with control gilts (20.5+/-0.3 d). When gilts received a single i.m. injection of 0 or 1 mg of estradiol valerate on d 11 and twice daily i.m. injections of 0 or 20 USP units OT on d 10 to 16 after estrus, an interaction (P = 0.05) between OT and estradiol valerate was detected. In the absence of exogenous estradiol valerate, injection of OT decreased interestrous interval (19.0+/-0.5 d) compared with injection of vehicle (20.4+/-0.5 d). However, when gilts were injected with 1 mg of estradiol valerate to inhibit luteolysis, OT did not prevent the increase in interestrous interval (25.4+/-0.5 d) compared with injections of vehicle (24.7+/-0.5 d). These results indicate that 1) exogenous OT administered by intrauterine infusion on d 10 to 16 did not decrease interestrous interval of intact cyclic gilts, 2) exogenous OT administered i.m. on d 10 to 16 shortened interestrous interval, and 3) exogenous OT did not prevent the increase in interestrous interval induced by estradiol valerate.