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Twenty female and castrated male crossbred meat goats (113 [+ or -] 7 d of age) were fed one of two diets to determine if poultry litter can be used as a suitable protein source in diets for meat goats. Animals were fed either a control, commercial diet (75% commercial diet, 25% alfalfa pellets), or a poultry litter-based diet (40% poultry litter, 35% corn and 25 % alfalfa pellets) with 3 pens/treatment and 10 goats/treatment. Animals that had been exposed to creep feed while nursing were weaned and placed in an indoor facility with 8 X 8 pens and slatted concrete floors and allowed ad libitum access to feed, water and minerals. The goats were allowed a 14-d adjustment period in which they were gradually introduced to the treatment diet such that at the end of the adjustment period, goats were receiving 100% of the treatment diet and no digestive problems were observed. Goats were weighed weekly and feed consumption determined biweekly for the eight-week trial. Total gain for goats on the control diet (20.1 [+ or -] 3.26 kg) was greater (P < 0.05) than for those receiving the poultry litter-based diet (6.2 [+ or -] 1.52 kg). Feed efficiency (gain/feed) for the control group (0.12 [+ or -] 0.04) was not different from animals receiving the poultry litter-based diet (0.07 [+ or -] 04). In summary, goats fed a commercial goat diet gained faster but had a similar feed efficiency when compared to goats fed the poultry litter-based diet. However, it was observed that goats were sorting the poultry litter-based diet, so further studies are needed using a pelleted diet to minimize sorting. Also, it is important to note that near the end of the study, two animals receiving the poultry litter-based diet died of urinary calculi. Key Words: Meat goat, Poultry litter, Feed intake

Ability to select service sires that minimize partial or complete losses of pregnancy could have major economic impacts in sheep production systems. This study tested the null hypothesis that survival of potential progeny did not vary with breed type of service sire or among individual rams. Data included 980 ewes on 10 farms; each ewe was pregnant to 1 of 67 rams of 12 breeds. Number of conceptuses was estimated once during pregnancy by ultrasonography, either transrectal (embryos) or transabdominal (fetuses), and was compared with number of lambs born to estimate losses. Data were examined first for number of lambs born and second for documented losses. Individual service sires affected number born (P < 0.001), which varied from 0.70 to 2.45 lambs per pregnant ewe. The main effects of breed type on lambs born were not significant, but breed types of both service sires (P < 0.0002) and ewes (P < 0.001) interacted with diagnosed number of conceptuses. Lambs born varied with ewe age (P < 0.0001) and among farms (P < 0.0001), and statistically, farms interacted with number of diagnosed conceptuses (P < 0.0001); season had no effect. In documented losses, there were both main effects of individual service sire and a service sire × number of diagnosed embryos interaction (P < 0.005). Thus, ewes bred to some rams were more apt to lose single pregnancies, whereas ewes bred to other rams were more apt to lose 1 or more embryos or fetuses from multiple pregnancies. Breed type of service sire affected (P < 0.05) prenatal death. Complete losses of single conceptuses tended to be greater in ewes bred to black-faced or hair-type rams (service sire breed type × number of diagnosed conceptuses; P < 0.09). Breed type of ewes also varied in incidence of complete losses (P < 0.05); hair-type ewes (46%) lost more (P < 0.02) documented conceptuses from examination to birth than black-faced (27%), white-faced (20%), or dairy-type (25%) ewes. Greater losses of singles than of multiples occurred in black-faced (37% vs. 18%) and hair-type (64% vs. 27%) ewes than in other breeds (ewe breed type × number of conceptuses; P < 0.03) per ewe. Surprisingly, purebred conceptuses were lost less often (24%) than crossbreds (36.4%; P < 0.002). Selection of rams based on records of prenatal losses in ewes they serviced may be a method to decrease embryonic and fetal wastage. However, further study to determine repeatability of differences among service sires from year to year will be required.

Twenty-one mixed-parity (average 2.4 +/- 0.49) crossbred sows and their offspring were used to determine whether sow milk leptin at farrowing was related to neonatal serum leptin and pig growth to weaning. During farrowing, pigs were randomly allotted to suckling (n = 99) or delayed suckling (n = 89) groups, with delayed suckling pigs placed in a group pen apart from the dam before suckling. Both groups had access to heat lamps. Colostrum samples were collected no more than 2 h after farrowing the first pig. Blood samples were collected from all pigs approximately 2 h after farrowing was complete; pigs were then ear notched and returned to their dams. Pig BW was recorded at 1.2 +/- 0.04 d of age and again at weaning. Milk and blood serum were collected after centrifugation; leptin concentrations were estimated using RIA. Leptin was detected in colostral milk, as expected, and averaged 46.0 +/- 1.1 ng/mL. Pig serum leptin (P < 0.02) was greater in suckling pigs than in delayed suckling pigs, averaging 0.69 +/- 0.08 and 0.54 +/- 0.07 ng/mL, respectively. Although male pigs were heavier (P < 0.01) at birth than female pigs (1,507 +/- 52 vs. 1,381 +/- 43 g), ADG to weaning and weaning weights were similar for both sexes, averaging 229 +/- 14 g and 5,829 +/- 323 g, respectively, for all pigs; serum leptin concentrations were not affected by sex of the pig. Milk serum leptin was not associated with litter size, parity, pig birth weight, ADG to weaning, or weaning weight. Suckling status did not influence ADG to weaning or weaning weight of pigs; neonatal pig serum leptin was not related to birth weight, weaning weight, or ADG to weaning. These results indicate that leptin is not directly related to early neonatal growth in the pig; however, more in-depth studies are needed to determine possible indirect or long-term effects of early leptin exposure.

Sixty-three Boer crossbred goats were used in 5 separate experiments (Exp. 1 to 5) to evaluate the effects of a commercial probiotic supplement on growth performance (Exp. 1 to 4), diet digestibility (Exp. 5), carcass traits (Exp. 3), and fecal bacterial populations (Exp. 4). Goats were either fed a commercially pelleted concentrate diet and supplemented with a commercial probiotic (PRO) that had shown anecdotal positive effects on goat growth and performance according to local goat producers, or they remained as controls. The dose of PRO used was within the labeled dose for sheep for all studies. For Exp. 1, goat BW and feed intake were measured and G:F was calculated every 7 d for 56 d. For Exp. 2 to 4, BW and feed intake were measured and G:F was calculated every 14 d. The first day of supplementation was considered d 0. Carcass traits were also collected at slaughter on d 57 for Exp. 3, and fecal samples were collected every 14 d for microbial culture for Exp. 4. For Exp. 5, which was a digestibility trial that lasted for 10 d, animals were placed in metabolic pens for collection of feces and orts. Growth performance of goats was not affected by probiotic supplementation, with the exception of performance in Exp. 2, in which ADG and G:F were improved (P < 0.03) in PRO goats compared with control goats on d 56 only (treatment x day interaction; P < 0.05), averaging 0.21 +/- 0.02 kg/d for PRO goats and 0.11 +/- 0.02 kg/d for control goats for ADG and 0.17 +/- 0.02 for PRO goats and 0.10 +/- 0.02 for control goats for G:F. Carcass weights and weights of fabricated cuts (shoulder, loin, leg, rack, shank, and total parts) as well as carcass length, leg circumference, loin eye area, and backfat were not influenced by PRO supplementation. Apparent digestibilities of OM, DM, NDF, ADF, CP, and GE (on a DM basis) were similar for the PRO and control treatments. Fecal culture analysis of Escherichia coli and coliforms, Lactobacillus, and Bifidobacterium populations were not influenced by the PRO treatment. Overall, although the PRO treatment affected goat ADG and G:F in Exp. 2, no PRO treatment effects were noted on growth performance for Exp. 1, 3, and 4. Furthermore, the PRO treatment did not affect diet digestibility, carcass traits, or fecal microbial populations in goats. In conclusion, no consistent benefits were noted from supplementing healthy, growing meat goats with PRO.

Boer and Boer crossbred meat-type does were used in two experiments to determine whether goat milk serum contains leptin and to investigate possible correlations of milk and serum leptin in does and subsequent growth of their offspring. Blood and milk samples were collected within 2 h of kidding (d 0) from 20 (Exp. 1; spring) or 22 does (Exp. 2; the following fall). Blood milk samples were then collected again on d 0.5, 1, 3, 5, 7, 14, 21, 28, 35, 42, 49, and 56 (Exp. 1) or d 0.5, 1, 2, 3, 4, 5, 6, 7, 14, and 21 (Exp. 2). Body weights of kids were recorded on d 0, and BW of kids and does were recorded weekly beginning on d 7 (kids) or 21 (does), with BCS also recorded for does beginning on d 28 for Exp. 1 and on d 0.5, 1, 2, 3, 4, 5, 6, 7, 14, and 21 for Exp. 2. Leptin was detected in colostral milk and was influenced by days postpartum, decreasing (P < 0.001) over time with an average of 4.4 +/- 0.3 ng/mL (Exp. 1) and 18.1 +/- 1.0 ng/mL (Exp. 2) on d 0 compared with 1.0 +/- 0.3 ng/mL on d 56 (Exp. 1) and 2.9 +/- 0.2 ng/mL on d 21 (Exp. 2). Day postpartum and milk serum leptin were negatively correlated (P < 0.001) for Exp. 1 (r = -0.27) and Exp. 2 (r = -0.46). For Exp. 1 only, blood serum leptin tended (P = 0.09) to be influenced by day, with a weak positive correlation (r = 0.15; P < 0.02). Weak positive correlations (P < 0.01) were found between blood serum leptin and doe BCS (r = 0.42 in Exp. 1, and r = 0.13 in Exp. 2) and doe BW (r = 0.44 in Exp. 1, and r = 0.26 in Exp. 2), with the absence of a stronger relationship likely due in part to the short time period measured and the lack of significant changes in BCS and BW during that time. In conclusion, leptin was present in milk and blood serum of does, and blood serum leptin was weakly correlated with doe BW and BCS, but it was not related to kid BW. Therefore, further studies are needed to clarify the relationships involving milk and serum leptin in goats.

Estrus synchronization allows for parturition at suitable times to take advantage of niche markets, feed supplies, labor, and rising price trends. In the past, synchronization of estrus in goats has focused primarily on dairy goats to allow for optimal timing of milk production. However, recent interest in meat goat production has resulted in attempts to use dairy goat, sheep, and cattle synchronization regimens in meat goat management systems. Methods of synchronization have included techniques as simple as alteration of light patterns or manipulation of social inputs (i.e., the buck effect) and as complex as varying timed hormonal treatments combined with light alteration and the buck effect. The synchronization of estrus using timed hormonal treatments seems to be more convenient in many meat goat production situations. Examples of hormones used include melatonin, progestogens (administered orally, as an injection, or by using intravaginal releasing devices), gonadotropins/GnRH (or agonists), and PG alone or in combination. As is seen with sheep and cattle, breed and/or breed type, stage of production, and environmental effects can influence synchronization success in goats. The introduction of breeds developed in other countries for rapid growth, such as the Boer goat, and increased consumer and producer interest have added to the impetus for developing cost-efficient and highly effective estrus synchronization regimens. New research is being conducted and various synchronization methods are being attempted in goats, a minor species, and the objective of this paper is to review these efforts.

Obesity has been a major concern in the horse industry for many years, and the recent discovery of leptin and leptin receptors in numerous nonequine species has provided a basis for new approaches to study this problem in equine. The objectives were to: 1) clone a partial sequence ofthe equine leptin and leptin receptor genes so as to enable the design of primers for RT-PCR determination of leptin and leptin receptor gene presence and distribution in tissues, 2) develop a radioimmunoassay to quantify peripheral concentrations of leptin in equine, 3) determine if peripheral concentrations of leptin correlate with body condition scores in equine, and 4) determine if changing body condition scores would influence peripheral concentrations of leptin in equine. In Experiment 1, equine leptin (GenBank accession number AF179275) and the long-form of the equine leptin receptor (GenBank accession number AF139663) genes were partially sequenced. Equine leptin receptor mRNA was detected in liver, lung, testis, ovary, choroid plexus, hypothalamus, and subcutaneous adipose tissues using RT-PCR. In Experiment 2, 71 horses were categorized by gender, age, and body condition score and blood samples were collected. Sera were assayed for leptin using a heterologous leptin radioimmunoassay developed for equine sera. Serum concentrations of leptin increased in horses with body condition score (1 = thin to 9 = fat; r = 0.64; P = 0.0001). Furthermore, serum concentrations of leptin were greater in geldings and stallions than in mares (P = 0.0002), and tended to increase with age of the animal (P = 0.08). In Experiment 3, blood samples, body weights, and body condition scores were collected every 14 d from 18 pony mares assigned to gain or lose weight over a 14-wk interval based on initial body condition score. Although statistical changes (P = 0.001) in body condition scores were achieved, congruent statistical changes in peripheral concentrations of leptin were not observed, likely due to the small range of change that occurred. Nonetheless, serum concentrations of leptin tended to be greater in fat-restricted mares than in thin-supplemented mares (P = 0.09). We conclude that leptin and leptin receptors are present in equine tissues and that peripheral concentrations of leptin reflect a significant influence of fat mass in equine.

In three experiments, the influence of insulin administered after weaning was examined in primiparous sows given extra feed or in primiparous compared to multiparous sows. In Exp. 1, 171 primiparous and 231 multiparous crossbred sows on a commercial farm were injected with 0.4 IU/kg BW insulin (Eli Lilly Lente Iletin II) or saline for 4 d beginning the day after weaning (d 0) and were fed 2.3 kg/d until mating. In Exp. 2, 153 primiparous sows from the same farm as those in Exp. 1 were injected with insulin or saline as in Exp. 1 and were fed 2.7 or 3.6 kg/d until mating. In Exp. 3, 63 primiparous crossbred sows were injected with insulin or saline as described above and fed either 2.3 or 4.5 kg/d for 5 d after weaning and were remated. On the commercial farm (Exp. 1 and 2), insulin administration increased percentage in estrus for primiparous sows compared to multiparous sows (treatment x parity interaction, P < 0.02) but tended to lower litter size in primiparous sows (treatment x parity interaction, P < 0.06). In Exp. 2, insulin combined with extra feed increased (P < 0.05) litter size by two pigs but tended (P < 0.07) to decrease farrowing rate in that group (treatment x feed interaction). Weaning-to-estrus interval, pregnancy rate, ovulation rate, and embryo survival were not influenced by treatment or feeding level (Exp. 3); however, postweaning intake and embryo survival were negatively related for saline-treated sows only (r = -0.55; P < 0.01), and backfat depth at weaning and embryo survival were positively related for insulin-treated sows only (r = 0.44; P < 0.05). Overall, insulin administration differentially influenced reproduction in primiparous sows and may have interacted with metabolic or nutritional state of the animal.

Leptin is an adipocyte-derived hormone that suppresses feed intake and increases energy expenditure. Leptin is also involved in regulating body temperature. Thus, the presence of leptin in milk, which can be absorbed through the gut of neonates immediately after birth, may aid in the survival of neonates born in cold weather. Our objectives were to determine the temporal relationship between concentrations of leptin in postpartum ewe blood serum and ewe milk serum, and to determine whether ewe blood and milk serum leptin concentrations were correlated with concentrations of leptin in lamb blood serum in their off-spring. Approximately 1 wk before the expected date of lambing, blood samples, weights, and body condition scores (BCS; 0 to 5 scale) were collected from 27 mixed-parity ewes. Following parturition, ewe blood and milk samples were collected within 2 h of parturition (d 0), 12 h (d 0.5) and 24 h (d 1) after parturition, again on d 5, and weekly thereafter until d 47. Lambs were blood-sampled and weighed within 2 h of parturition (d 0), bled daily until d 5, and bled and weighed weekly thereafter to d 47. Prior to lambing, ewe blood serum leptin was positively correlated with congruent BCS (r2 = 0, 10, P = 0.06), but not weight (P = 0.14). Following parturition, ewe blood serum leptin was positively correlated with BCS, weight, and milk serum leptin (r2 = 0.14, P < 0.0001, r2 = 0.12, P < 0.0001, and r2 = 0.028, P = 0.04). Leptin in milk serum was correlated with ewe weight (r2=0.05, P = 0.007) but not ewe BCS (P = 0.7); however, concentrations of leptin in both ewe blood and milk serum varied with day of lactation (P = 0.0001), being maximal within 24 h of parturition and declining to nadir concentrations by d 5. Leptin in lamb serum was correlated with milk serum leptin, (r2 = -0.05; P = 0.001), but not ewe blood serum leptin (P = 0.5). Concentrations of leptin in lamb serum increased from birth to d 5 and declined thereafter to nadir concentrations by d 19. Elevated concentrations of leptin in milk during the early stages of lactation may provide a mechanism for thermoregulation, satiation, and homeostatic endocrine control in the neonate.

We compared the effects of exogenous insulin and porcine ST (pST) on follicular development after weaning. Crossbred primiparous sows received saline (1.5 mL i.m.; n = 9), insulin (.4 IU/kg BW s.c.; Eli Lilly Lente Iletin II; n = 10), or pST (40 microg/kg BW i.m.; n = 10) from d 1 to 5 after weaning (d 0). Ovaries were collected, the diameter of each follicle > or = 2 mm was measured, and fluid from the 20 largest follicles was assessed for IGF-I, IGF binding proteins (IGFBP), estradiol, progesterone, and testosterone. The total number (27.7, 25.3, and 29.1 for saline, insulin, and pST, respectively; SEM = 3.2) and average diameter (4.7, 5.2, and 5.5 mm for saline, insulin, and pST treatments, respectively; SEM = .3 mm) of ovarian follicles were not affected by insulin or pST treatment. The pST and insulin increased follicular fluid estradiol and testosterone in medium and large follicles compared to fluid from saline-treated sows, but the increase was greater for insulin than for pST treatment (treatment x size interaction, P < .01). Similarly, progesterone concentrations in follicular fluid were higher in medium and large follicles after insulin treatment, and pST treatment induced higher progesterone concentrations in small follicles and increasingly lower concentrations of progesterone in medium and large follicles (treatment x size interaction, P < .0007) compared to saline treatment. Follicular fluid IGF-I was greater (treatment x health interaction, P < .0001) in atretic and nonatretic follicles from pST-treated sows than in those from insulin- and saline-treated sows. Follicular fluid IGFBP-2 (tendency, P < .07) and IGFBP, possibly representing IGFBP-5 (30 kDa) and IGFBP-4 (22 kDa), were higher in atretic follicles than in nonatretic follicles (P < .05), whereas IGFBP-3 was not influenced by health status. The 30- and 22-kDa IGFBP were also influenced by treatment, increasing due to pST compared with saline or insulin treatments (P < .008). Follicular fluid IGFBP-2 and IGFBP-3 were not influenced by treatment. In conclusion, pST and insulin positively influenced follicular steroidogenesis and possibly follicular development, although through different mechanisms.

The relationship of excitatory amino acid (EAA) activity to LH secretion was investigated in ovariectomized crossbred prepuberal gilts (93 +/- 1 kg BW) and Yorkshire barrows (94 +/- 2 kg BW) in two experiments. In Exp. 1, eight gilts received, i.m., saline (S) or 20 mg of Ketamine (K)/kg BW, a noncompetitive EAA receptor antagonist. Within these groups, four then received 10 mg of N-methyl-DL-aspartate (NMA)/kg BW, an EAA agonist, or S i.v. Mean serum LH concentrations were similar among groups before treatment, did not change after S+S, but decreased (P < .05) by 1 h after S+NMA, 3 h after K+S, and 2 h after K+NMA. Serum cortisol concentrations did not change after S+S, but were increased (P < .05) from 30 to 90 min after S+NMA, at 120 min after K+S, and from 30 to 120 min after K+NMA. In Exp. 2, barrows received 2.5 mg of NMA/kg BW i.v. immediately after i.m. injection of S (n = 7) or 19.9 mg of K/kg BW (n = 8). Mean serum LH concentrations for the 2 h before treatment were similar among barrows, but decreased (P < .05) by 2 h after K+NMA and was not altered after S+NMA. Serum cortisol concentrations were increased at 30 min after S+NMA and from 60 to 90 min after K+NMA. We suggest that EAA both inhibit and stimulate LH secretion, with the inhibitory effects lying within the basal hypothalamus and the stimulatory effects lying within higher brain centers.