Biomedical subjects

C R Barb

Publications and source records attributed to C R Barb.

At least 37 records · Page 2Linked to original sources

PubMed2001

Nutritional regulators of the hypothalamic-pituitary axis in pigs.

Nutritional signals are detected by the central nervous system (CNS) and translated by the neuroendocrine system into signals that alter secretion of LH and growth hormone (GH). Furthermore, these signals directly affect the activity of the pituitary gland independently of CNS input. Insulin-like growth factor I (IGF-I), insulin, leptin and specific metabolites, such as glucose and free fatty acids (FFA), are potential signals of the metabolic status to the brain-pituitary axis. Intravenous injection of a lipid emulsion or glucose suppressed the GH and LH response to GH releasing hormone (GHRH) and GnRH, respectively. Insulin and IGF-I regulation of LH and GH secretion occur at the pituitary gland. Feed deprivation for 24 h suppressed leptin secretion without affecting LH or GH secretion, whereas central administration of leptin resulted in a decrease in feed intake and an increase in GH secretion. Oestrogen-induced leptin gene expression in adipose tissue increased with age and adiposity in pigs. Leptin stimulated GnRH release from hypothalamic tissue in vitro. These results identify putative signals that link metabolic status and neuroendocrine control of growth and reproduction by altering endocrine function during periods of fasting, feed restriction and lactation.

Animal Nutritional Physiological Phenomena↗

PubMed2000

Effect of testosterone on n-methyl-d, l-aspartate-induced growth hormone secretion in male swine.

Previous research from our laboratory demonstrated that n-methyl-d, l-aspartate (NMA), a potent agonist of glutamate, increased growth hormone (GH) secretion in barrows and boars. To determine if testosterone modulates NMA-induced GH secretion, Poland China x Yorkshire swine were challenged with NMA in a model that compared GH responses in boars with those of barrows or barrows treated with testosterone propionate (TP). Boars and barrows weighing 112.6+/-1.4 kg (mean +/- SE) were fitted with indwelling jugular vein catheters. Barrows (n = 16) were given i.m. injections of TP (25 mg in corn oil) twice daily from d 0 to d 6. Boars (n = 16) and control barrows (n = 15) received twice daily injections of corn oil. On d 6, blood was sampled every 15 min for 4 h. Two h after sampling began, all animals received an i.v. injection of NMA at a dose of 2.5 mg/kg body weight. Mean testosterone concentrations (ng/ml serum) were similar (P > .1) for boars (8.1+/-0.8) and barrows receiving TP (7.3+/-0.3), but were greater in both cases (P < .05) than for barrows receiving corn oil (.2+/-.01). Prior to NMA injections, mean GH concentrations were similar (P > .1) among groups and averaged 2.7+/-.2 ng/ml serum across treatments. Serum concentrations of GH after NMA increased (P < .05) similarly among groups and averaged 6.3+/-0.3 ng/ml across treatments during the 2-h period after injection. These results were not supportive of a role for testosterone as a modulator of NMA-induced GH secretion in male swine.

Animals↗

PubMed2000

Luteinizing hormone response to controlled-release deslorelin in estradiol benzoate primed ovariectomized gilts.

Development of a controlled release formulation of gonadotropin releasing hormone that would stimulate a LH surge capable of reducing the time span of ovulations would greatly benefit reproductive management because a single timed insemination could be used. A dose-response study was conducted to determine if Deslorelin, a potent gonadotropin releasing hormone analogue, delivered via the SABER system, a biodegradable controlled release system, would stimulate an ovulatory-like LH surge in the pig. Twenty ovariectomized gilts, approximately 200 d old and 100 kg body weight (BW), received estradiol benzoate (15 microg/kg BW im) and 48 h later, the gilts were given deslorelin at 0, 12.5, 25.0, 50.0 or 100.0 microg im (n = 4 each treatment group). Compared to controls, mean blood deslorelin concentrations were still elevated at 30 h after deslorelin. Mean deslorelin magnitude, area under the curve and duration were sequentially greater (P<0.05) in a dose-dependent sequence. Compared to controls, serum LH concentrations were elevated (P<0.05) for 6 to 12 h after deslorelin. A dose-response relationship was absent for all parameters of LH secretion. Magnitude of the serum LH response was greatest (P<0.05) in the 12.5 microg and 50.0 microg groups, whereas area under the curve was lower (P<0.05) after 25.0 microg of deslorelin than after 12.5, 50.0 and 100.0 microg, which were not different from each other. Thus, no more than 12.5 microg of deslorelin is necessary to obtain maximum LH release in the model studied and doses less than 12.5 microg may also be effective.

Animals↗

PubMed2000

Long form leptin receptor mRNA expression in the brain, pituitary, and other tissues in the pig.

Much effort has focused recently on understanding the role of leptin, the obese gene product secreted by adipocytes, in regulating growth and reproduction in rodents, humans and domestic animals. We previously demonstrated that leptin inhibited feed intake and stimulated growth hormone (GH) and luteinizing hormone (LH) secretion in the pig. This study was conducted to determine the location of long form leptin receptor (Ob-Rl) mRNA in various tissues of the pig. The leptin receptor has several splice variants in the human and mouse, but Ob-Rl is the major form capable of signal transduction. The Ob-Rl is expressed primarily in the hypothalamus of the human and rodents, but has been located in other tissues as well. In the present study, a partial porcine Ob-Rl cDNA, cloned in our laboratory and specific to the intracellular domain, was used to evaluate the Ob-Rl mRNA expression by RT-PCR in the brain and other tissues in three 105 d-old prepuberal gilts and in a 50 d-old fetus. In 105 d-old gilts, Ob-Rl mRNA was expressed in the hypothalamus, cerebral cortex, amygdala, thalamus, cerebellum, area postrema and anterior pituitary. In addition, Ob-Rl mRNA was expressed in ovary, uterine body, liver, kidney, pancreas, adrenal gland, heart, spleen, lung, intestine, bone marrow, muscle and adipose tissue. However, expression was absent in the thyroid, thymus, superior vena cava, aorta, spinal cord, uterine horn and oviduct. In the 50 d-old fetus, Ob-Rl mRNA was expressed in brain, intestine, muscle, fat, heart, liver and umbilical cord. These results support the idea that leptin might play a role in regulating numerous physiological functions.

Animals↗

PubMed2000

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↗

PubMed2000

Concentrations of leptin in serum and milk collected from lactating sows differing in body condition.

Leptin concentrations in the circulation and milk were determined in sows that differed in body condition at farrowing, and in feed consumption during lactation. Serum concentrations of leptin at farrowing and weaning were highest in sows exhibiting the greatest amount of backfat. Leptin was detected in both skim and whole milk throughout lactation, but levels were not correlated with backfat thickness or circulating leptin concentrations. This report provides the first evidence for the presence of leptin in sow milk; its function in the physiology of suckling pigs remains to be determined.

Adipose Tissue↗

PubMed2000

Growth performance and adipose tissue deposition in barrows fed n-methyl-D,L-aspartate.

We previously reported that broilers fed n-methyl-D,L-aspartate (NMA) exhibited enhanced feed conversion efficiency and decreased percentage of fat in carcasses. In this experiment, growth performance and backfat thickness were evaluated in barrows fed NMA. Poland China x Yorkshire barrows weighing 68.8 +/- 1.7 kg (mean +/- SE) were allowed ad libitum access to feed containing NMA at levels of either 0 (n = 7), 100 (n = 6), 200 (n = 8), or 300 (n = 8) mg/kg for 36 d. Barrows were slaughtered at 99.5 +/- 2.3 kg BW. There was no effect (P > 0.1) of NMA on ADG or feed consumption. Gain:feed ratio decreased (P < 0.03) in a linear fashion with increasing level of NMA. There was a cubic effect (P < 0.05) of NMA treatment on first-rib backfat thickness. In response to graded levels of NMA, backfat thickness at the 10th rib (P < 0.08) and last rib (P < 0.03) increased in a linear fashion. The NMA had no effect (P > 0.1) on backfat thickness measured at the lumbar vertebra or longissimus muscle area measured at the 10th rib interface. The percentage of lean in the carcass decreased in a linear fashion (P < 0.05) in response to increasing levels of NMA in the diet. In summary, NMA had an overall negative effect on growth performance and carcass yield characteristics in barrows. The dichotomous effects of NMA on feed efficiency and body composition in poultry and swine warrants further scrutiny.

Adipose Tissue↗

PubMed2000

Serum concentrations of luteinizing hormone, growth hormone, testosterone, estradiol, and leptin in boars treated with n-methyl-D,L-aspartate.

Three experiments were conducted to determine the effects of n-methyl-D,L-aspartate (NMA), an agonist of the excitatory amino acid glutamate, on secretion of hormones in boars. In Exp. 1, boars (185.0+/-.3 d of age; mean +/- SE) received i.v. injections of either 0, 1.25, 2.5, 5, or 10 mg of NMA/kg BW. There were no effects of NMA (P>.1) on secretion of LH and testosterone. Treatment with NMA, however, increased (P<.01) circulating GH concentrations in a dose-dependent manner. In Exp. 2, boars (401 d of age) received an i.v. challenge of NMA at a dose of 10 mg/kg BW or .9% saline. Treatment with NMA, but not saline (P>.1), increased serum concentrations of LH (P<.01), GH (P <.01), and testosterone (P<.06). In Exp. 3, boars that were 152, 221, or 336 d of age were treated i.v. with NMA (10 mg/kg BW). Across ages, treatment with NMA increased circulating concentrations of LH (P<.07) and testosterone (P<.01). However, NMA increased (P<.01) mean GH concentrations in only the oldest boars. Treatment with NMA had no effect (P>.1) on circulating concentrations of estradiol or leptin; however, estradiol concentrations increased (P<.03) with age. In summary, NMA increased secretion of LH, GH, and testosterone in boars. However, endocrine responses to treatment with NMA may be influenced by age of the animal. Finally, NMA did not influence circulating concentrations of estradiol or leptin.

Age Factors↗

PubMed1999

Effect of cysteamine hydrochloride on secretion of growth hormone in male swine.

The objective of this study was to determine the effect of cysteamine hydrochloride (CSH) on growth hormone (GH) secretion in male swine. Twelve Poland China x Yorkshire boars, weighing 103.4 +/- 3.0 kg and fitted with indwelling jugular vein catheters, were individually penned in an environmentally controlled room. Boars received i.v. injections of either 0, 25, 50, or 75 mg CSH/kg body weight (BW) at h 0 (n = 3/treatment). Blood samples were collected every 15 min from h 0 to h 4. Serum concentrations of GH were determined by radioimmunoassay. There was an effect of treatment (P < .05) on mean GH concentrations. Mean GH concentrations (ng/ml) were 1.97 +/- .46, 2.24 +/- .59, .91 +/- .06, and .62 +/- .08 for boars receiving 0, 25, 50, and 75 mg CSH/kg BW, respectively. The dose of CSH-mean GH response had a linear (P < .01) component. Cysteamine hydrochloride at the 75 mg/kg BW dose decreased mean GH concentrations (P < .05) compared to the 0 and 25 mg/kg BW groups. The frequency and amplitude of GH pulses were similar (P > .1) among treatments. Overall, GH pulse amplitude was 2.35 +/- .58 ng/ml and GH pulse frequency was .75 +/- .07 pulses/h. Results from this experiment indicate that CSH suppresses circulating GH concentrations in a dose dependent fashion in boars.

Animals↗

PubMed1999

Leptin mRNA expression and serum leptin concentrations as influenced by age, weight, and estradiol in pigs.

Two experiments (EXP) were conducted to determine the roles of age, weight and estradiol (E) treatment on serum leptin concentrations and leptin gene expression. In EXP I, jugular blood samples were collected from gilts at 42 to 49 (n = 8), 105 to 112 (n = 8) and 140 to 154 (n = 8) d of age. Serum leptin concentrations increased (P < 0.05) with age and averaged 0.66, 2.7, and 3.0 ng/ml (pooled SE 0.21) for the 42- to 49-, 105- to 112-, and 140- to 154-d-old gilts, respectively. In EXP II, RNase protection assays were used to assess leptin mRNA in adipose tissue of ovariectomized gilts at 90 (n = 12), 150 (n = 11) or 210 (n = 12) d of age. Six pigs from each age group received estradiol (E) osmotic pump implants and the remaining animals received vehicle control implants (C; Day 0). On Day 7, back fat and blood samples were collected. Estradiol treatment resulted in greater (P < 0.05) serum E levels in E (9 +/- 1 pg/ml) than C (3 +/- 1 pg/ml) pigs. Serum leptin concentrations were not affected by age, nor E treatment. Leptin mRNA expression was not increased by age in C pigs nor by F in 90- and 150-d-old pigs. However, by 210 d of age, leptin mRNA expression was 2.5-fold greater (P < 0.01) in E-treated pigs compared to C animals. Serum insulin concentrations were similar between treatments for 210-d-old pigs. However, insulin concentrations were greater (P < 0.05) in E than C pigs at 90 d and greater in C than E animals at 150 d. Plasma glucose and serum insulin-like growth factor-I concentrations were not influenced by treatment. These results demonstrate that serum leptin concentrations increased with age and E-induced leptin mRNA expression is age- and weight-dependent.

Adipose Tissue↗

PubMed1999

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↗

PubMed1999

Expression of beta-galactosidase and pig leptin gene in vitro by recombinant adenovirus.

Adenovirus has been used in vivo and in vitro as a vector to carry a foreign gene for gene transfer. Two kinds of replication defective human recombinant adenovirus vectors were used in this study, the first containing beta-galactosidase reporter gene (AdCMVLac-Z) and the second carrying a gene for porcine leptin gene (AdCMVpLeptin). AdCMVLac-Z was tested for its ability to transfer DNA into pig kidney and pituitary cells. These cells expressed Lac-Z transiently 48 hours after the infection. In addition, when the pig kidney cells expressing the Lac-Z were replated with low density for the formation of colonies from each cell, colonies of blue cells expressing Lac-Z were observed. These results demonstrate that human recombinant adenovirus can be used as a transducing viral vector for inducing long-term expression in pig kidney cells. We also constructed a recombinant adenovirus (AdCMVpLeptin) which contained a pig leptin gene for the expression of pig leptin in vitro in the 293 human kidney cell line. 293 cells transfected with AdCMVpLeptin produced both a 15 KDa of a secretory form of porcine leptin and an 18 KDa long form containing signal peptide. Our study demonstrated that the recombinant adenovirus system offers a method for gene transfer and expression in pig cells.

Adenoviridae↗

PubMed1999

The brain-pituitary-adipocyte axis: role of leptin in modulating neuroendocrine function.

The recently discovered protein leptin has a molecular mass of 16 kDa, consists of 146 amino acids, and is synthesized and secreted by adipose tissue. Leptin affects feed intake, the neuroendocrine-axis, and immunological processes. The protein was first identified as the gene product that is deficient in the obese ob/ob mouse. Leptin serves as a circulating signal of nutritional status and plays a pivotal role in regulation of body weight, energy expenditure, growth, and reproduction.

Adipocytes↗

PubMed1998

Delay of estradiol-induced surge secretion of LH in gilts by intracerebroventricular injection of morphine.

In Experiment 1, ovariectomized (OVX) gilts, 143 d old and 58.5 +/- 1.8 kg BW, received 10 micrograms estradiol benzoate (EB)/kg BW i.m. and either 500 micrograms of the endogenous opioid peptide (EOP) agonist, morphine (MOR), in saline (SAL; n = 5), or SAL (n = 4) intracerebro-ventricularly at 40 and 48 hr after EB. With the exception of one MOR-treated gilt, which was deleted from Experiment 1, LH secretion was suppressed for at least 50 hr in all gilts. Timing of the LH surge was similar among gilts. However, total LH secreted was greater (P < 0.05) after SAL than MOR. The experiment was repeated at 179 d of age and 78.6 +/- 1.2 kg BW, except that treatments were reversed among gilts. Emergence of the LH surge was delayed (P < 0.005) by 10.8 hr and time to maximum LH concentration (P < 0.05) by 6.8 hr after MOR than after SAL. Magnitude and total LH secreted were not different among gilts. In Experiment 2, gilts which had displayed estrous cycles of 18-22 d were OVX and treated as in Experiment 1, except MOR (n = 3) or SAL (n = 4) were injected 10 hr later than in Experiment 1, i.e., at 50 and 58 hr after EB. Secretion of LH was suppressed for at least 60 hr in both groups. Time to emergence of the LH surge was delayed by 27 hr (P < 0.05) after MOR compared to after SAL. However, other parameters of the surge were not different among gilts. Thus, EOP modulate LH surge secretion negatively in the pig.

Animals↗

PubMed1998

Recombinant porcine leptin reduces feed intake and stimulates growth hormone secretion in swine.

Two experiments (EXP) were conducted to test the hypothesis that porcine leptin affects GH, insulin-like growth factor-I (IGF-I), insulin, thyroxine (T4) secretion, and feed intake. In EXP I, prepuberal gilts received intracerebroventricular (i.c.v.) leptin injections. Blood was collected every 15 min for 4 hr before and 3 hr after i.c.v. injections of 0.9% saline (S; n = 3), 10 micrograms (n = 4), 50 micrograms (n = 4), or 100 micrograms (n = 4) of leptin in S. Pigs were fed each day at 0800 and 1700 hr over a 2-wk period before the EXP. On the day of the EXP, pigs were fed at 0800 hr and blood sampling started at 0900 h. After the last sample was collected, feeders were placed in all pens. Feed intake was monitored at 4, 20, and 44 hr after feed presentation. In EXP II, pituitary cells from prepuberal gilts were studied in primary culture to determine if leptin affects GH secretion at the level of the pituitary. On Day 4 of culture, 10(5) cells/well were challenged with 10(-12), 10(-10), 10(-8), or 10(-6) M [Ala15]-h growth hormone-releasing factor-(1-29)NH2 (GRF), 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(-8) and 10(-6) M GRF. Secreted GH was measured at 4 hr after treatment. In EXP I, before injection, serum GH concentrations were similar. Serum GH concentrations increased (P < 0.01) after injection of 10 micrograms (21 +/- 1 ng/ml), 50 micrograms (9 +/- 1 ng/ml), and 100 micrograms (13 +/- 1 ng/ml) of leptin compared with S (1 +/- 2 ng/ml) treated pigs. The GH response to leptin was greater (P < 0.001) in 10 micrograms than 50 or 100 micrograms leptin-treated pigs. By 20 hr the 10, 50, and 100 micrograms doses of leptin reduced feed intake by 53% (P < 0.08), 76%, and 90% (P < 0.05), respectively, compared with S pigs. Serum IGF-1, insulin, T4, glucose, and free fatty acids were unaffected by leptin treatment. In EXP II, relative to control (31 +/- 2 ng/well), 10(-10), 10(-8), and 10(-6) M GRF increased (P < 0.01) GH secretion by 131%, 156%, and 170%, respectively. Only 10(-6) M and 10(-7) M leptin increased (P < 0.01) GH secretion. Addition of 10(-11) and 10(-9) M leptin in combination with 10(-6) M GRF or 10(-11) M leptin in combination with 10(-8) M GRF-suppressed (P < 0.05) GH secretion. These results indicate that leptin modulates GH secretion and, as shown in other species, leptin suppressed feed intake in the pig.

Animals↗

PubMed1998

Evidence for a luteinizing hormone surge center in the hypothalamus of the pig.

Studies were conducted to determine whether there is an LH surge generator in the hypothalamus of the pig. In experiment 1, 157-day-old ovariectomized (OVX) gilts received 1.5 microg estradiol benzoate (EB)/kg BW i.m. every 12 h from 0 through 24, 48, 72, or 96 h. Blood was sampled every 6 h from 3 to 36 h and every 3 h from 36 through 144 h. One of 3, 4 of 4, 4 of 4, and 2 of 3 gilts displayed an LH surge after treatment for 24, 48, 72, and 96 h, respectively. With the exception that time to maximum LH concentration was greater in gilts treated for 96 h than in those treated for 72 h (p < 0.05), parameters of the surge were similar among all gilts. In experiment 2a, an Alzet osmotic pump containing EB or vehicle was inserted s.c. behind an ear of 124-day-old OVX gilts, resulting in the following daily doses of EB: 0, 0.75, 1.50, or 3.00 microg/kg BW. Blood was sampled at 0, 2, 4, 6, and 8 h and every 8 h thereafter through 168 h to evaluate surge secretion of LH, and every 15 min for 8 h starting at 168 h to evaluate pulsatile LH secretion. Zero of 3, 0 of 2, 3 of 3, and 3 of 3 gilts displayed an LH surge after 0, 0.75, 1.50, and 3.00 microg EB/kg BW, respectively. Parameters of the surge were similar among gilts. Pulsatile LH secretion, evaluated 7 days after pump insertion, was significantly suppressed for estradiol-treated gilts compared to controls. In experiment 2b, at 182 days of age, 10 gilts used in experiment 2a plus 2 additional gilts in the original group prepared but not used for experiment 2a, were randomly assigned in groups (n=3) to the following daily doses of EB: 0, 0.19, 0.38, or 0.75 microg/kg BW, administered again by osmotic pump. Treatment and blood-sampling schedules were the same as in experiment 2a. Zero, 0, 1, and 2 gilts displayed an LH surge after treatment with 0, 0.19, 0.38, and 0.75 microg EB/kg BW, respectively. Parameters of the surge were similar among gilts that displayed an LH surge. Pulsatile LH secretion was significantly suppressed for estradiol-treated gilts compared to controls. Thus, the LH surge resulted from positive feedback stimulation of a specific surge generator rather than attenuation or dissipation of negative feedback inhibition of estradiol on a pulse generator.

Animals↗

PubMed1998

Serum concentrations of luteinizing hormone, growth hormone, and cortisol in gilts treated with N-methyl-D,L-aspartate during the estrous cycle or after ovariectomy.

The objective of this experiment was to determine the effects of n-methyl-d,l-aspartate (NMA), an agonist of the neurotransmitter glutamate, on circulating concentrations of LH, GH, and cortisol in gilts treated during the luteal (n = 4) or follicular (n = 4) phase of the estrous cycle, or after ovariectomy (n = 4). Blood was sampled every 15 min for 10 h on each of two consecutive days. On the 1st d, two gilts from each group received i.v. injections of NMA (10 mg/kg BW) at h 4 and 6, and the remaining gilts received .9% saline (vehicle). The following day, gilts that had received NMA on the 1st d received vehicle, and gilts that had received vehicle on d 1 received NMA. All gilts received an i.v. challenge of GnRH (.1 microg/kg BW) at h 8 on each day. The NMA treatment increased (P < .01) LH pulse frequency in luteal-phase gilts by 125%. In contrast, NMA decreased (P < .05) mean concentrations of LH by 48% and suppressed (P < .01) LH pulse frequency by 33% in ovariectomized gilts. No characteristics of LH secretion were affected (P > .05) by NMA in follicular phase gilts. Serum LH concentrations for the 2-h period following GnRH were lower (P < .05) in follicular-phase gilts than in ovariectomized gilts and were 1.15 +/- .09 (mean +/- SE), .81 +/- .05, and .51 +/- .17 ng/mL for ovariectomized, luteal-phase, and follicular-phase gilts, respectively. Treatment with NMA increased circulating concentrations of GH by 334% (P < .01) and cortisol by 77% (P < .03) in all gilts. We suggest that the effects of NMA on LH release in gilts depend on the circulating steroidal milieu. In contrast, NMA evokes secretion of GH and cortisol irrespective of the reproductive status of treated gilts.

Animals↗

PubMed1997

Nitrogen metabolism and hormonal responses of steers fed wheat silage and infused with amino acids or casein.

Four Holstein steers (159 kg) surgically fitted with abomasal-infusion cannulas were used in a 4 x 4 Latin square study to test amino acid (AA) and casein (CAS) infusions on nitrogen balance and hormonal status of steers consuming vegetative wheat (Triticum aestivum L.) silage (12.3% CP). Treatments were 5-d infusions of 1) water (CONT), 2) arginine (ARG; 13.69 g/d), 3) limiting amino acids (LAA, 13.69 g/d arginine + 10.92 g/d histidine + 28.97 g/d lysine + 10.88 g/d methionine + 16.96 g/d threonine, and 4) Na-CAS (300 g/d). Whole blood was collected for plasma AA, growth hormone (GH), insulin, and IGF-I concentrations. Data were analyzed by ANOVA, and the following orthogonal contrasts were used to separate treatment means: CONT vs ARG; ARG vs LAA; and LAA vs CAS. Urinary N increased (P < .02) for CAS vs LAA. Arginine increased N retention, as did CAS, compared to LAA. Total plasma essential AA were decreased by arginine. Mean plasma insulin concentrations were increased by CAS (P < .034). Arginine increased mean plasma GH levels, but not IGF-I. The CAS treatment increased (P < .015) IGF-I levels, but not GH. These data suggest that performance of steers fed wheat silage was limited by duodenal AA flow and that arginine was the first-limiting AA. Casein infusion increased plasma insulin and IGF-I, which would explain the improved growth noted in calves and lambs fed forages supplemented with ruminally undegraded protein.

Amino Acids↗