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J B Barrett

Publications and source records attributed to J B Barrett.

18 recordsLinked to original sources

Neuropeptide Y modulates growth hormone but not luteinizing hormone secretion from prepuberal gilt anterior pituitary cells in culture.

Pituitary cells, from seven 160- to 170-day-old pigs, were studied in primary culture to determine the affects NPY on LH and GH secretion at the level of the pituitary. On day 4 of culture, medium was discarded, plates were rinsed twice with serum-free medium and cells were cultured in 1 ml fresh medium without serum and challenged individually with 10(-10), 10(-8) or 10(-6) M [Ala(15)]-h growth hormone-releasing factor-(1-29)NH(2) (GRF); 10(-9), 10(-8) or 10(-7) M GnRH or 10(-9), 10(-8), 10(-7) or 10(-6) M NPY individually or in combinations with 10(-9) or 10(-8) M GnRH or 10(-8) or 10(-6)M GRF. Cells were exposed to treatment for 4 h at which time medium was harvested and quantified for LH and GH. Basal LH secretion (control; n = 7 pituitaries) was 12 +/- 6 ng/well. Relative to control at 4 h, 10(-9), 10(-8) and 10(-7) M GnRH increased (P < 0.01) LH secretion by 169, 176 and 197%, respectively. Neuropeptide-Y did not alter (P > 0.4) basal LH secretion nor 10(-8) M GnRH-induced increase in LH secretion but 10(-9) M GnRH-stimulated LH secretion was reduced by NPY and was not different from control or GnRH alone. Basal GH secretion (control; n = 7 pituitaries) was 56 +/- 12 ng/well. Relative to control at 4 h, 10(-10), 10(-8) and 10(-6) M GRF increased GH secretion by 111%, 125% (P < 0.01) and 150% (P < 0.01), respectively. Only 10(-6) M (134%) and 10(-7) M (125%) NPY increased (P < 0.04) basal GH secretion. Addition of 10(-9), 10(-8) and 10(-7) M NPY in combination with 10(-8) M GRF suppressed (P < 0.04) GRF-stimulated GH secretion. However, 10(-9) M NPY enhanced (P < 0.06) the GH response to 10(-6) M GRF. These results demonstrate that NPY may directly modulate GH secretion at the level of the pituitary gland.

Analysis of Variance↗

High-level aminoglycoside resistant enterococci isolated from swine.

Approximately 42% (187/444) of swine enterococci collected between the years 1999 and 2000 exhibited high-level resistance to gentamicin (MIC > or =500 microg/ml), kanamycin (MIC > or =500 microg/ml), or streptomycin (MIC > or =1000 microg/ml). Eight aminoglycoside resistance genes were detected using PCR, most frequently ant(6)-Ia and aac(6')-Ii from Enterococcus faecium. Twenty-four per cent (45/187) of total high-level aminoglycoside-resistant isolates and 26% (4/15) of isolates resistant to high levels of all three antimicrobials were negative for all genes tested. These data suggest that enterococci isolated from swine contain diverse and possibly unidentified aminoglycoside resistance genes.

Aminoglycosides↗

Role of leptin in modulating the hypothalamic-pituitary axis and luteinizing hormone secretion in the prepuberal gilt.

Three experiments (EXP) were conducted to test the hypothesis that leptin modulates LH, GnRH, and neuropeptide Y (NPY) secretion. In EXP I, prepuberal gilts received intracerebroventricular (i.c.v.) leptin injections and blood samples were collected. In EXP II, anterior pituitary cells from prepuberal gilts in primary culture were challenged with 10(-14), 10(-13), 10(-12), 10(-11), 10(-10), 10(-9), 10(-8), 10(-7), or 10(-6) M leptin individually or in combinations with 10(-10), 10(-9), and 10(-8) M GnRH. In EXP III, hypothalamic-preoptic area (HYP-POA) explants were placed in perfusion system and exposed to 0 (n=5), 10(-12) M (n=4), 10(-10) M (n=4), 10(-8) M (n=4), or 10(-6) M (n=5) human recombinant leptin (LEP) for 30 min. In EXP I, serum LH concentrations were unaffected by leptin treatment. In EXP II, all doses of leptin increased LH secretion except for 10(-12) and 10(-7) M. Only 10(-7), or 10(-13) M leptin in combination with 10(-8) or 10(-9) M GnRH, respectively, suppressed LH secretion. In EXP III, prior to leptin, media GnRH concentrations were similar across treatments. Media GnRH concentrations increased after 10(-12), 10(-10), and 10(-8) M leptin compared to control. Leptin treatment failed to influence NPY secretion across treatments. These results indicate that components of the neuroendocrine axis that regulate GnRH and LH secretion are functional and leptin sensitive before the onset of puberty. Other neural peptides in addition to NPY may mediate the acute effects of leptin on the GnRH-LH system and lastly, the inability of i.c.v. leptin treatment to increase LH secretion may in part be related to stage of sexual maturation and associated change in negative feedback action of estradiol on LH secretion.

Animals↗

The role of melanocortin-3 and -4 receptor in regulating appetite, energy homeostasis and neuroendocrine function in the pig.

A recently discovered class of receptors, melanocortin-3 and -4 receptor (MC3/4-R), are located within the brain and modulate feed intake in rodents. Stimulation of the receptor (agonist) inhibits feed intake whereas blockade (antagonist) of the receptor increases intake. Our knowledge of factors regulating voluntary feed intake in humans and domestic animals is very limited. i.c.v. administration of an MC3/4-R agonist, NDP-MSH, suppressed (P<0.05) feed intake compared with controls at 12, 24, 48 and 72 h after treatment in growing pigs. Fed pigs were more responsive to the MC3/4-R agonist then fasted animals. However, i.c.v. treatment with MC3/4-R antagonist, SHU9119, failed to stimulate intake. The failure of MC3/4-R antagonist to stimulate feed intake suggests involvement of other brain hormone(s) which antagonize the action of SHU9119 at the MC3/4-R, blocking its stimulatory effect on intake. Treatment with NDP-MSH or SHU9119, across a wide dose range, failed to affect LH and GH secretion, except for the 10 micro g dose of NDP-MSH, which exhibited both a stimulatory and an inhibitory effect on GH secretion in fasted animals. Treatment with agouti-related peptide, a natural brain hormone that blocks the MC3/4R, failed to stimulate feed intake. These results do not support the idea that endogenous melanocortin pays a critical role in regulating feed intake and pituitary hormone secretion in the pig. SHU9119 blocked the NDP-MSH-induced increase in cAMP in HEK293 cells expressing the porcine MC4-R sequence without the missense mutation. The EC(50) and IC(50) values were similar to the human MC4-R, confirming that SHU9119 is a pig MC4-R antagonist. However, pigs were heterozygous for an MC4-R gene missense mutation. It is possible that the MC4-R mutation alters function and this may explain the failure to demonstrate MC3/4-R involvement in modulating feeding behavior and LH and GH secretion in the pig.

Animals↗

Effects of N-methyl-D,L-aspartate on LH, GH, and testosterone secretion in goat bucks maintained under long or short photoperiods.

Photoperiod modulates reproduction in goats. We tested the hypothesis that the excitatory glutamatergic tone is reduced in the photoinhibited goat. The objectives of this study were to determine the effect of photoperiod and glutamatergic stimulation on LH, GH, and testosterone (T) secretion in goat bucks. Eight mature, intact bucks were used in two simultaneous 4 x 4 Latin square designs. Variables were two photoperiod regimens (short day; SD, 10 h light:14 h dark, n = 4; vs long day; LD, 16 h light:8 h dark, n = 4) and four doses of N-methyl-D-L-aspartate (NMA; 0, 1, 2 and 4 mg/kg BW, i.v.). Venous blood was obtained for 2 h before and after NMA injection, followed by GnRH injection and then a final 1 h of sampling. Injection of NMA increased (P < 0.002) LH secretion within 20 min. This increase was sustained for 120 min, but the response was most pronounced in LD goats. The increase in mean LH was associated with a concomitant dose-dependent increase in pulse frequency (P < 0.006). However, NMA treatment had no effect (P > 0.10) on LH pulse amplitude. The release of LH after injection of GnRH was not affected by photoperiod. Exposure of bucks to LD reduced T secretion relative to that of SD bucks (P < 0.01). However, GH secretion was enhanced in LD bucks (P< 0.001). The response of GH to NMA was dependent on photoperiod history. A highly significant immediate and sustained increase (P < 0.001) was observed in LD but not in SD bucks within 10 min. Overall, a dose-dependent increase (P < 0.01) in T secretion was stimulated by NMA in both LD and SD bucks. These results indicate that NMA receptors may be involved in the regulation of LH, GH, and testosterone secretion in the goat. Furthermore, length of day influences GH secretion in the goat and NMA receptor activation had divergent effects on the secretion of this hormone.

Animals↗

Serum leptin concentrations, luteinizing hormone and growth hormone secretion during feed and metabolic fuel restriction in the prepuberal gilt.

Two experiments were conducted to determine 1) the effect of acute feed deprivation on leptin secretion and 2) if the effect of metabolic fuel restriction on LH and GH secretion is associated with changes in serum leptin concentrations. Experiment (EXP) I, seven crossbred prepuberal gilts, 66 +/- 1 kg body weight (BW) and 130 d of age were used. All pigs were fed ad libitum. On the day of the EXP, feed was removed from four of the pigs at 0800 (time = 0) and pigs remained without feed for 28 hr. Blood samples were collected every 10 min from zero to 4 hr = Period (P) 1, 12 to 16 hr = P 2, and 24 to 28 hr = P 3 after feed removal. At hr 28 fasted animals were presented with feed and blood samples collected for an additional 2 hr = P 4. EXP II, gilts, averaging 140 d of age (n = 15) and which had been ovariectomized, were individually penned in an environmentally controlled building and exposed to a constant ambient temperature of 22 C and 12:12 hr light: dark photoperiod. Pigs were fed daily at 0700 hr. Gilts were randomly assigned to the following treatments: saline (S, n = 7), 100 (n = 4), or 300 (n = 4) mg/kg BW of 2-deoxy-D-glucose (2DG), a competitive inhibitor of glycolysis, in saline iv. Blood samples were collected every 15 min for 2 hr before and 5 hr after treatment. Blood samples from EXP I and II were assayed for LH, GH and leptin by RIA. Selected samples were quantified for glucose, insulin and free fatty acids (FFA). In EXP I, fasting reduced (P < 0.04) leptin pulse frequency by P 3. Plasma glucose concentrations were reduced (P < 0.02) throughout the fast compared to fed animals, where as serum insulin concentrations did not decrease (P < 0.02) until P 3. Serum FFA concentrations increased (P < 0.02) by P 2 and remained elevated. Subcutaneous back fat thickness was similar among pigs. Serum IGF-I concentration decreased (P < 0.01) by P 2 in fasted animals compared to fed animals and remained lower through periods 3 and 4. Serum LH and GH concentrations were not effected by fast. Realimentation resulted in a marked increase in serum glucose (P < 0.02), insulin (P < 0.02), serum GH (P < 0.01) concentrations and leptin pulse frequency (P < 0.01). EXP II treatment did not alter serum insulin levels but increased (P < 0.01) plasma glucose concentrations in the 300 mg 2DG group. Serum leptin concentrations were 4.0 +/- 0.1, 2.8 +/- 0.2, and 4.9 +/- 0.2 ng/ml for S, 100 and 300 mg 2DG pigs respectively, prior to treatment and remained unchanged following treatment. Serum IGF-I concentrations were not effected by treatment. The 300 mg dose of 2DG increased (P < 0.0001) mean GH concentrations (2.0 +/- 0.2 ng/ml) compared to S (0.8 +/- 0.2 ng/ml) and 100 mg 2DG (0.7 +/- 0.2 ng/ml). Frequency and amplitude of GH pulses were unaffected. However, number of LH pulses/5 hr were decreased (P < 0.01) by the 300 mg dose of 2DG (1.8 +/- 0.5) compared to S (4.0 +/- 0.4) and the 100 mg dose of 2DG (4.5 +/- 0.5). Mean serum LH concentrations and amplitude of LH pulses were unaffected. These results suggest that acute effects of energy deprivation on LH and GH secretion are independent of changes in serum leptin concentrations.

Animals↗

Feed intake and serum GH, LH and cortisol in gilts after intracerebroventricular or intravenous injection of urocortin.

In three experiments (Exp), ovariectomized gilts received intracerebroventricular (ICV; Exp 1 - with restraint, Exp 2 - without restraint) or intravenous (i.v.; Exp 3) injections of urocortin or saline to assess effects on feed intake and serum GH, LH, and cortisol. Following a 20-hr fast, feed was presented at 1 hr (Exp 1) or 30 min (Exp 2 and 3) after injection (time = 0 hr) of saline or 5 (U5) or 50 (U50) microg/pig (Exp 1 and 2) or 5 microg/kg BW (Exp 3) of urocortin. Blood samples were collected every 15 min from -2 to 6 hr relative to injection and hormone data pooled 2 hr before and hourly after treatment. Treatment with U50 decreased feed intake, relative to saline (treatment x time interaction; P < 0.05), when delivered ICV but not i.v. A treatment by time interaction was detected for GH (Exp 1, 2, 3) and LH (Exp 1 and 2; P < 0.01). Serum GH increased over time (relative to -2 hr; P < 0.05) following treatment with urocortin but not saline regardless of route of administration. Conversely, in Exp 1 (U5 and U50) and Exp 2 (U50), LH decreased relative to -2 hr with a delayed decrease during Exp 1. Serum cortisol was not affected by treatment in Exp 1, but increased following urocortin in Exp 2 and 3 (treatment by time interaction, P < 0.01). These data provide evidence that urocortin modulates GH and LH concentrations and suppresses feed intake in gilts via mechanisms which may be independent of cortisol and may depend upon dose and route of administration.

Adrenocorticotropic Hormone↗

Effects of N-methyl-D, L-aspartate on secretion of growth hormone-releasing hormone from the boar hypothalamic-preoptic area and median eminence in vitro.

N-methyl-D, L-aspartate (NMA) elicited secretion of growth hormone (GH)-releasing hormone from both the hypothalamic-preoptic area and the median eminence that were collected from boars. We suggest that the previously described increase in GH secretion that follows peripheral treatment of swine with NMA is attributable, at least in part, to NMA-stimulated secretion of GH-releasing hormone from the central nervous system.

Animals↗

N-methyl-D,L-aspartate modulation of luteinizing hormone and growth hormone secretion from pig pituitary cells in culture.

Administration of n-methyl-d, l-aspartate (NMA) to pigs in vivo increased GH and suppressed LH secretion. Cultures of anterior pituitary cells from pigs in the follicular phase (FOL; n = 3) and luteal phase (LUT; n = 3) of the estrous cycle, and ovariectomized (OVX; n = 10) pigs were treated with NMA (10(-4), 10(-6) or 10(-8) M) or the NMA antagonist, 2-amino-5-phosphonopentanoic acid (AP5; 10(-4), 10(-6) or 10(-8) M), to determine if NMA affects the pituitary directly. Secreted LH and GH were measured at 4 h after treatment. Basal LH and GH secretion (control; C) were 1.1 +/- 0.6, 4.4 +/- 2.1 and 5.6 +/- 1.3 ng/well and 5.2 +/- 1.2, 7.5 +/- 1.2 and 5.2 +/- 1.7 ng/well for FOL, LUT and OVX, respectively. Relative to C, 10(-4) M NMA increased (P < 0.001) LH secretion 2.4-, 2.2- and 5.1-fold in FOL, LUT and OVX cultures, respectively. The effect of 10(-4) M NMA was inhibited by 10(-4) M AP5 (P < 0.05) in FOL cultures, but not in OVX cultures. GnRH increased (P < 0.001) LH levels 3.1-, 2.3- and 3.8-fold in FOL, LUT and OVX cultures, respectively. Relative to C, 10(-4), 10(-6) and 10(-8) M NMA increased (P < 0.03) GH secretion 1.5-, 1.5- and 2.3-fold in LUT and 1.7-, 2.3- 2.0-fold in OVX cultures, respectively. AP5 alone or in combination with NMA failed to alter basal GH secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Serum glucose and free fatty acids modulate growth hormone and luteinizing hormone secretion in the pig.

Two experiments were conducted to determine the effect of free fatty acids (FFA) and glucose treatment on growth hormone (GH) and luteinizing hormone secretion in the pig. In Experiment (Exp) 1, 15 prepuberal gilts received an intravenous infusion of FFA (n = 5; 3 ml of 10% Liposyn II/kg), glucose (n = 5; 1 g/kg), or saline (n = 5; 3 ml of 0.9%/kg). Jugular blood samples were collected every 15 min for 2 hr before and 3 hr after intravenous infusion of saline, FFA, and glucose. Synthetic [Ala15]-h growth hormone-releasing factor-(1-29)NH2 (1 microgram/kg) and gonadotropin-releasing hormone (0.2 micrograms/kg) were administered 30 min after infusion (Time 0 = infusion). In Exp 2, eight prepuberal gilts received either FFA (n = 4) or saline (n = 4) as described in Exp 1, except that treatments were given every hour ove a 10-hr period. Blood samples were collected every 15 min from 1 hr before to 10 hr after the start of FFA or saline infusion. In Exp 1, the peak GH response to growth hormone-releasing factor was delayed by 45 min (P less than 0.01) by glucose treatment and suppressed (P less than 0.01) by FFA treatment. The luteinizing hormone response to gonadotroph-releasing hormone was suppressed (P less than 0.03) by glucose and enhanced (P less than 0.03) by FFA. In Exp 2, the number of GH pulses was increased (P less than 0.05) by FFA infusion and GH concentrations were positively correlated (r = 0.58, P less than 0.0003) with FFA concentrations, while luteinizing hormone pulse amplitude was greater (P less than 0.01) in FFA gilts than in saline gilts. These results indicate that FFA are more effective modulators of GH secretion than acute hyperglycemia, while metabolic status can alter pituitary responsiveness to gonadotropin-releasing hormone.

Animals↗

Opioid modulation of LH secretion by pig pituitary cells in vitro.

The effects of naloxone and beta-endorphin on LH secretion by pig pituitary cells were studied in primary cultures. On Day 4 of culture, cells (10(5) seeded/well) were challenged with 10(-9), 10(-8) or 10(-7) M gonadotrophin-releasing hormone (GnRH), 10(-10), 10(-9), 10(-8) or 10(-7) M-beta-endorphin or 10(-6) M-naloxone individually or in combinations. Secreted LH was measured at 4 h and 24 h after treatment and cellular content of LH was measured after 24 h. Basal LH secretion (control) was 23.5 +/- 7.6 and 36.9 +/- 10.3 ng/well at 4 h and 24 h, respectively. Relative to control at 4 h, 10(-9), 10(-8) or 10(-7) M-GnRH stimulated (P less than 0.05) LH secretion 140%, 210% and 250%, respectively. At 24 h, LH secretion was increased (P less than 0.05) by GnRH compared to control, but the dose-response to GnRH was absent. Naloxone increased (P less than 0.01) LH secretion 166 +/- 13% at 4 h and 141 +/- 13% (P less than 0.06) at 24 h. Secretion of LH after simultaneous addition of 10(-8) M-GnRH plus naloxone was greater (P less than 0.01) than after GnRH alone at 4 h but not at 24 h. beta-Endorphin at 10(-10), 10(-9), 10(-8) or 10(-7) M failed to alter basal LH secretion at 4 h but decreased secretion at 24 h, while cellular LH content was similar to control at 24 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Composition and muscle cellularity of Japanese Quail after selection for high body weight under an optimal or suboptimal nutritional environment.

The purpose of this study was to determine if the compositional and cellularity changes associated with selection for rapid growth rate in an optimal and suboptimal nutritional environment were similar. The P-line Japanese quail had undergone long-term selection for high 4-week body weight and received a 28% protein diet. The unselected C-line quail received the same diet. T-line quail were selected by the same criteria as P-line quail but received a 20% protein diet containing .2% thiouracil. Body weights and muscle weights of P- and T-line quail were similar at 10 days of age. At 56 days T-line body weight and muscle weights were intermediate between C- and P-line quail, but whole body composition of P- and T-line quail was similar. The P- and T-line quail possessed a greater apparent number of muscle fibers than C line quail. Total muscle DNA content was lower in T-line muscles compared to P-line muscles at 56 days of age. No differences within age were observed among lines of myofiber diameter, fiber type composition, for concentrations of DNA, RNA and protein, or for protein/DNA and RNA/DNA. At 10 days the weight, length and diameter of the humerus and femur bones were greatest in T-line quail; these same parameters were intermediate between C- and P-line quail at 28 and 56 days of age. It was concluded that selection for rapid growth rate per se caused apparent fiber number and fiber length to increase while the effect of suboptimal nutritional environment was not evident until after 10 days of age. Selection under suboptimal conditions as exercised in this study prevented expression of the maximum number of muscle DNA units.

Animals↗

Green hair.

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Adolescent↗