Two experiments were conducted to examine influences of dietary energy and insulin on ovulation rate and patterns of luteinizing hormone (LH), follicle stimulating hormone (FSH), glucose, insulin and estradiol in gilts during 6 d before estrus. In Exp. 1, 36 gilts were given altrenogest for 14 d to synchronize estrus. In a factorial arrangement, gilts were fed one of two levels of dietary energy (5,771 or 9,960 kcal metabolizable energy (ME)/d), and given one of two levels of porcine insulin (0 or .1 IU/kg body weight iv every 6 h). Dietary treatments began 4 d before and insulin treatments began 1 d after the last day of altrenogest, respectively, and lasted until 24 h after estrus. Main effect means for number of corpora lutea were 14.0 +/- 1.3 and 17.6 +/- .9 for 5,771 and 9,960 kcal ME (P less than .05), and 14.6 +/- 1.0 and 17.0 +/- .9 for 0 and .1 IU insulin (P less than .05). Number of LH peaks on d 3 was greater for gilts that received 9,960 kcal than 5,771 kcal (3.3 +/- .2 vs 2.7 +/- .2; P less than .05), and for .1 than 0 IU insulin (3.2 +/- .2 vs 2.7 +/- .2; P less than .05). During the first 24 h of sampling, concentrations of LH and FSH were greater (P less than .05) in gilts receiving 9,960 kcal ME plus insulin than for other treatment combinations. Concentrations of estradiol were not affected by treatments. In Exp. 2, two formulations of insulin were evaluated for influence on ovulation rate. All gilts received altrenogest and 9,960 kcal ME/d as in Exp. 1. Then on the first day after altrenogest, seven gilts each received short-acting insulin (as in Exp. 1), long-acting insulin (zinc suspension, 1.0 IU/kg body weight every 18 to 24 h), or served as controls. Ovulation rates were increased (P less than .05) by both insulin preparations (15.6, control; 19.1, short-acting; 18.5, long-acting; SE = 1.2). Concentrations of LH tended to be greater after short-acting insulin, but differences were not significant (P = .13). We conclude that increases in ovulation rate produced by dietary energy and insulin are not necessarily accompanied by changes in gonadotropins or estradiol.

The influence of excitatory amino acids (EAA) on growth hormone (GH) secretion and the possible site of action was investigated in the pig. In Experiment (Exp) I three replicates were conducted with 30 prepuberal gilts, 130 d of age and averaging 70.6 +/- 1.3 kg body weight (BW). Six gilts each received intravenously (i.v.) 0, 50, 100, or 150 mg/kg BW of aspartate (ASP) or glutamate (GLU) in saline. Blood samples were collected every 15 min for 2 hr before and 3 hr after treatment. In Exp II, mature ovariectomized gilts (163 +/- 10 kg BW) that had been immunized against growth hormone releasing factor (GRF) conjugated to human serum albumin (GRFi; n = 4) or against human serum albumin alone (HSAi; n = 5) received 150 mg/kg BW ASP or GLU i.v. in a 2 x 2 factorial arrangement of treatments, which was then repeated in a crossover design. One week later, all animals received 10 mg/kg N-methyl-D,L-aspartate (NMA; EAA agonist) in saline i.v. Blood samples were collected as described above. In Exp III, cultures of anterior pituitary cells from market-weight (averaging 105 kg BW) gilts were studied. On Day 4 of culture, cells (10(5) seeded/well) were challenged with 10(-8), 10(-6), or 10(-4) M ASP or GLU, 10(-6) M [Ala15]-human GRF (1-29)-NH2, or the EAA antagonist, 2-amino-5-phosphonopentanoic acid (10(-4) M; AP5), alone or in combination with ASP or GLU. In Exp I, all doses of ASP and the 100- and 150-mg doses of GLU increased (P < 0.05) GH secretion when compared with Time 0. However, serum GH concentrations were higher (P < 0.01) after 150 mg/kg of ASP when compared with those after 150 mg/kg of GLU. In Exp II, serum GH concentrations increased (P < 0.05) in HSAi but not in GRFi pigs (averaging 1.2 +/- 0.2 ng/ml before and 8.2 +/- 0.7, 6.3 +/- 0.5, and 9.2 +/- 0.5 ng/ml by 15 min after ASP, GLU, and NMA, respectively). In Exp III, relative to controls (40 +/- 6 ng/ml), GH increased (P < 0.05)1.6-, 1.9-, and 1.9-fold and 1.7-, 1.8-, and 2.0-fold after 10(-8), 10(-6), and 10(-4) M ASP and GLU, respectively. The EAA receptor antagonist AP5 failed to prevent the GH response to ASP or GLU, except for 10(-8) M ASP. In summary, ASP is a more potent secretagogue of GH secretion than is GLU in vivo, whereas each is equipotent in vitro. Because no stimulation of GH by EAA was observed in GRFi pigs and no specific dose-response effect of EAA was found in vitro, it may be concluded that modulation by EAA is mediated primarily at the level of the hypothalamus or higher brain centers.

No abstract

The effects of exogenous naloxone and adrenocorticotropin (ACTH) on circulating concentrations of corticosterone and glucose in broilers were determined. Birds were injected i.m. at 0 and 2 h with either saline or naloxone, then i.v. at 2.5 h with either saline or ACTH. Control birds received saline at each injection. Blood samples were taken before the experiment started (0 min) and 30, 60, and 90 min after the last injection. Intramuscular injections of naloxone significantly reduced subsequent ACTH-stimulated increases in serum corticosterone; however, when followed by saline, naloxone elevated corticosterone by 90 min after the final injection of saline. Glucose levels were significantly elevated at 60 min in birds receiving ACTH i.v., but remained elevated through 90 min in birds pretreated with naloxone. Naloxone pretreatment attenuated serum corticosterone but augmented serum glucose concentrations in ACTH-stimulated broilers.