Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HORMONES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 325 records · Page 18Linked to original sources
PubMed1988

Simultaneous measurement of gonadotropin-releasing hormone, luteinizing hormone, and follicle-stimulating hormone in the orchidectomized rat.

In the present study two recently developed techniques have been combined to enable the simultaneous in vivo determination of pulsatile release of GnRH, LH, and FSH in the orchidectomized rat. The first of these techniques involves the implantation of two vascular catheters and collecting serial blood samples through one while simultaneously infusing a replacement blood mixture through the other; consequently, blood samples can be collected for an extended period of time, and detailed plasma LH and FSH release profiles can be established for individual animals. The second technique involves push-pull perfusion of the pituitary gland to determine changes in GnRH concentration as might be perceived by the gonadotropes. For each animal (n = 6), blood (150 microliters) and push-pull perfusate (200 microliters) samples were collected at 5- and 10-min intervals, respectively, for approximately 6 h, and the hormone release profiles were determined by RIA. All of the rats showed a clear pulsatile release pattern for GnRH, LH, and FSH. Moreover, the interpulse interval was remarkably similar for each of these hormones (36.9, 41.5, and 43.5 min, respectively, as determined by PULSAR). The percentage of GnRH pulses associated with a gonadotropin pulse was 72% for LH and 76% for FSH; only 14% of the pulses were silent for both gonadotropins. These results demonstrate that in the orchidectomized rat the pulsatile pattern of GnRH release is reflected in the pulsatile pattern of not only LH but also FSH. They may, therefore, be construed to support the concept that the pulsatile secretion of both gonadotropins is primarily orchestrated by a single hypothalamic releasing hormone. Alternatively, if two separate hypothalamic releasing hormones do indeed exist (LHRH and FSH-releasing hormone), it would appear that in the orchidectomized rat their episodic release is tightly coupled to the same hypothalamic pulse generator.

Animals↗
PubMed1991

[Pituitary and plasma levels of growth hormone (GH), follicle stimulating hormone (FSH) and luteinizing hormone (LH) in hereditary dwarf rats (rdw/rdw)].

Koto et al found a new hereditary dwarf mutation from breeding colony of Wistar-Imamichi rat and named 'rdw'. To characterize endocrinological functions in rdw rats, pituitary and plasma levels of pituitary hormones including growth hormone (GH), follicle stimulating hormone (FSH) and luteinizing hormone (LH) were compared between rdw and normal rats. The hormone levels were estimated with radioimmunoassay (RIA). It was found that pituitary and plasma levels of GH of rdw were drastically decreased and those of FSH and LH were inclined to decrease but not remarkable as compared with normal. Rats of rdw were, therefore, considered to be useful as a model animal for endocrinological defects.

Animals↗
PubMed1976

Interaction between oestrogen and gonadotrophin- releasing hormone on the release and synthesis of luteinizing hormone and follicle-stimulating hormone from incubated pituitaries.

The release and synthesis of LH and FSH were studied in adenohypophyses from ovariectomized rats incubated for a period of 4 h in flasks containing 1 ml Eagle's medium. One hemipituitary was used as the experimental gland and the other half served as a control. Glands from ovariectomized untreated animals showed a spontaneous release of LH and FSH and the amount of hormones released (per mg gland) by both the hemipituitaries was not significantly different. Also the content of the hormones at the end of the incubation period was similar in both halves. Gonadotrophin-releasing hormone (Gn-RH) added to the incubation medium stimulated the release of LH and FSH. A dose--response relationship was obtained between doses of 0-51 and 8-00 ng/ml medium. Although lower doses were required to increase the release of LH, the amount of FSH released was higher when expressed as a percentage of gland content. Pituitary glands from ovariectomized rats treated with 5 mug oestradiol benzoate 24 h before being killed showed an increase in sensitivity to Gn-RH, but the response decreased when oestrogen was injected 2 h before death. Also the addition of oestradiol-17beta to the incubation medium inhibited LH and FSH release induced by Gn-RH. Gonadotrophin-releasing hormone increased the spontaneous synthesis of LH and FSH observed in the incubated pituitaries. This effect of Gn-RH was stimulated by the injection of oestrogen into the donor animals whereas administration of oestrogen into the medium enhanced the synthesis of LH and partially inhibited that of FSH. These results provide evidence for a dual effect of oestrogen on the release of LH and FSH induced by Gn-RH. They also show that synthesis of gonadotrophic hormones was favoured by oestrogen or by increased gonadotrophin release.

Animals↗
PubMed1995

Effects of short-term cortisol infusion on growth hormone-releasing hormone stimulation of growth hormone release in sheep.

Excess production or long-term administration of glucocorticoids is detrimental to longitudinal growth in people and rats. A portion of this effect is attributed to cortisol inhibition of growth hormone (GH). Glucocorticoid effects are usually studied in subjects under long-term treatment with synthetic, more potent glucocorticoids, and, to the authors' knowledge, have not been examined in domestic animals. We sought to examine the effects of cortisol infusion on GH release in sheep. Cortisol infusion into castrated, male Suffolk sheep (1 to 1.5 years old) caused a significant (P < 0.0001) increase in cortisol concentration. Basal GH release was not affected over the 4-hour period of infusion. Growth hormone-releasing hormone administration stimulated GH release in both groups (P < 0.001); however, the control group had a greater response to growth hormone-releasing hormone than did the cortisol infused group (P < 0.0001). These results were duplicated in cultured sheep pituitary cells. Cortisol inhibition of GH release may be mediated via enhanced somatostatin release, owing to a direct inhibition of somatotrope function, or a combination of both mechanisms. Because of effects of stress and disease in increasing cortisol concentration, additional study of the mechanisms for cortisol inhibition of GH release in sheep needs to be performed.

Analysis of Variance↗
PubMed1994

[An immunocytochemical analysis of the hormonal status of animals transgenic for growth hormone genes and for a mini-gene of human growth hormone-releasing factor].

An immunocytochemical analysis of hormonal status of transgenic rats containing human growth hormone gene has been done. The enhanced expression of the endogenous growth hormone gene was demonstrated with poly- and monoclonal antibodies inside somatatropes of pituitary. No activity of the heterologous growth hormone gene was revealed in kidney, pancreas or liver as it might be expected according to specificity of MT1 and TAT promotors. Transgenic animals of F0, F1 and F2 generation exhibited disturbance of functional morphology of glucagon and insulin producing cells. Lymphocyte infiltration was found in pancreatic islets. The transgenic rabbits and swine with the gene of releasing factor of human growth hormone did not reveal any severe disturbance. Although one swine demonstrated alterations in glucagon producing cells and one rabbit revealed a disturbed morphology of the stomach tissues. The data are discussed in relation to general problems of transgene activity and interaction with endogenous homolog.

Animals↗
PubMed1984

Altered responses of prolactin, luteinizing hormone and follicle stimulating hormone secretion to thyrotrophin releasing hormone/gonadotrophin releasing hormone stimulation in cyclical mastalgia.

A generalized abnormality of hypothalamopituitary function was found in 17 patients with cyclical pronounced mastalgia compared with 11 controls by using a combined thyrotrophin releasing hormone and gonadotrophin releasing hormone test. The release of prolactin, luteinizing hormone and follicle stimulating hormone was significantly greater in cyclical mastalgia patients than in controls. Basal thyrotrophin, T3 and T4 levels were within the normal range in both groups indicating normal thyroid status in benign breast disease. The single measurement of oestrogen and progesterone in the luteal phase was not abnormal. These data demonstrate an alteration in lactotroph and gonadotroph function in patients with cyclical mastalgia. It is unknown at present whether this represents an appropriate cellular response to altered central or peripheral signals. There is no evidence to suggest, however, that the anterior pituitary cell types are abnormal per se.

Adult↗
PubMed2001

Growth hormone-releasing hormone and growth hormone secretagogue-receptor ligands: focus on reproductive system.

Growth hormone-releasing hormone (GHRH) and somatostatin are the most important hypothalamic neurohormones controlling growth hormone (GH) secretion. Several neurotransmitters and neuropeptides also play an important role in the control of GH secretion, mainly acting via modulation of GHRH and somatostatin. In the past two decades, particular attention has been given to a new family of substances showing a strong GH-releasing effect: GH secretagogues (GHSs). GHSs increase GH secretion in a dose- and age-related manner after iv and even oral administration. The endocrine effects of GHSs, are not fully specific for GH; they show, in fact, prolactin- (PRL), adenocorticotropic hormone- and cortisol-releasing effects. Specific GHS receptors are present in both the central nervous system and peripheral tissues, where they mediate several extraendocrine effects of GHSs. The isolation of these "orphan" receptors suggested the existence of an endogenous GHS-like ligand that could be represented by a recently discovered gastric peptide, named ghrelin. The interaction between GHSs and GHRH at the central level and in the pituitary gland, but not at peripheral level, has clearly been shown. Because GHRH and GHS receptors share the same localization in some peripheral tissues, they may have some interactions even at this level.

Adrenocorticotropic Hormone↗
PubMed2001

Hormonal and anthropometric predictors of bone mass in healthy elderly men: major effect of sex hormone binding globulin, parathyroid hormone and body weight.

Osteoporosis in men is a significant health problem, and factors associated with bone mass are being investigated. Although osteoporosis is a typical feature of hypogonadism, the influence of testosterone levels and other hormonal factors on bone mass of eugonadal males is unknown. Our aim was to identify several anthropometric and hormonal predictors that could be responsible for the variability in bone mineral density (BMD) in healthy men. One hundred elderly men (age 68 +/- 7 years) were investigated in this cross-sectional study. BMD was measured by dual-energy X-ray absorptiometry (DXA) at the lumbar spine and femoral sites (femoral neck, Ward's triangle, trochanter, intertrochanter and total femur). Anthropometric measures were obtained including: weight, height, body mass index (BMI), waist-hip ratio and testicular volume. Hormonal data measures were total, free and bioavailable testosterone, dihidrotestosterone, estradiol, sex hormone binding globulin (SHBG), insulin-like growth factor I (IGF-I), intact parathyroid hormone (iPTH) and 1,25-dihydroxyvitamin D3 (1,25(OH)2D3). One subject was excluded because primary hypogonadism was found. SHBG levels were increased in 53.5% of men, and 8% showed a mild increase in iPTH levels. Twenty-eight subjects had densitometric criteria of osteoporosis (T-score < or = -2.5). All BMD sites were positively correlated with body weight (r = 0.29-0.48, p < 0.001) and BMI (r = 0.24-0.47, p < 0.001). A negative correlation between SHBG levels and intertrochanter (IT) and total femur (TL) BMD was found (r = -0.24 and r = -0.22, p < 0.05). After adjusting for age and BMI, SHBG and IGF-I levels were negatively correlated (r = -0.33, p < 0.001). In multiple linear regression analysis independent predictors of bone mass were body weight, SHBG and iPTH levels. The best predictive model accounted for 24-40% of the observed variability of BMD. However, most of the BMD variability was explained by body weight. In conclusion, in our study body weight, SHBG and iPTH levels were predictors of BMD in healthy elderly men.

Absorptiometry, Photon↗
PubMed1985

Reevaluation of the relative activities of the pituitary glycoprotein hormones (follicle-stimulating hormone, luteinizing hormone, and thyrotrophin) from the green sea turtle, Chelonia mydas.

The discovery that the follicle-stimulating hormone (FSH) previously prepared from the green sea turtle, Chelonia mydas, contained a major neurohypophysial contaminant prompted a repurification and characterization of the glycoprotein hormones in this turtle. Results reaffirmed the physicochemical distinctiveness of the three hormones. Minimal cross-contamination between hormones (less than 2%) was achieved by ion-exchange chromatography, subunit dissociation (of contaminating luteinizing hormone (LH], gel filtration, and immuno-affinity chromatography. New preparations of FSH and thyrotrophin (TSH) derived from adult pituitaries proved to be more potent than those described previously (the degree depending on the nature of the assay); FSH showed the expected increase in activity based on estimated contamination of previous preparations. LH was similar to original preparations except for enhanced activity in FSH radioreceptor assays. Binding assays (in heterologous and homologous systems) again demonstrated the general absence of an FSH-specific receptor in the reptilian (chelonian and squamate) testes. In an in vivo bioassay in the lizard Anolis, the turtle FSH was orders of magnitude more potent than LH in stimulating both testis growth and androgen secretion, but in vitro LH was considerably more potent than FSH in stimulating androgen secretion in squamate and chelonian testes. Thus, the possibility exists that androgen secretion in some chelonian systems may exhibit a high degree of LH specificity like that of mammals and birds.

Androgens↗
PubMed1982

Growth hormone (GH), thyroid-stimulating hormone (TSH), and luteinizing hormone (LH)-like peptides in the rodent brain: non-parallel ontogenetic development with pituitary counterparts.

Brain and anterior pituitary growth hormone (GH), thyroid-stimulating hormone (TSH) and luteinizing hormone (LH) were measured during fetal, neonatal, and pubertal life and into adulthood. Immunoassayable GH and TSH could be found in the fetal whole brain before their detection in the fetal pituitary. Developmental patterns of pituitary and brain hormones differed in that pituitary hormones showed a gradual rise in levels from birth to puberty at approximately 20 days of age. Biochemically similar, brain-based peptides demonstrated a remarkable preparturitional surge in concentrations that was limited to a few days immediately preceding birth. Twenty-four hours after birth, brain GH, TSH, and LH had dropped to levels equal to or less than concentrations in the neonatal pituitary and subsequently rose to adult levels around the time of puberty. In these studies it could be shown that both the placental-fetal barrier and the neonatal blood-brain barrier were intact. These observations indicate the presence of two biochemically and immunologically similar but topographically distinct pools of peptides present in the developing brain and in the anterior pituitary gland.

Aging↗
PubMed1992

Height prognosis of children with true precocious puberty and growth hormone deficiency: effect of combination therapy with gonadotropin releasing hormone agonist and growth hormone.

We evaluated height prognosis and therapeutic efficacy of long-term, combination therapy with gonadotropin releasing-hormone agonist and growth hormone (GH) in five children (three girls) with coexistent precocious puberty and GH deficiency. Their clinical characteristics and growth response were compared with those of 12 girls with idiopathic true precocious puberty and eight prepubertal GH-deficient children (one girl). Precocious GH-deficient subjects were older than the precocious GH-sufficient children (9.5 +/- 1.8 years vs 6.5 +/- 1.3 years; mean +/- SD), but bone ages were comparable (12 +/- 3.7 years vs 10 +/- 0.9 years); their chronologic age was similar to that of the prepubertal GH-deficient children (9.6 +/- 2.1 years), but bone age was significantly more advanced (6.9 +/- 2.3 years). The mean height velocity of the prepubertal GH-deficient children (3.8 +/- 1.5 cm/yr) was lower than that of the precocious GH-deficient subjects (6.7 +/- 1.6 cm/yr) and the precocious GH-sufficient children (9.5 +/- 2.9 cm/yr). Baseline adult height prediction z scores were significantly lower in the precocious GH-deficient children (-3.7 +/- 1.0) than in either the precocious GH-sufficient children (-2.2 +/- 1.0) or the prepubertal GH-deficient subjects (-1.5 +/- 0.8). During therapy with gonadotropin releasing-hormone agonist, growth rates slowed to an average of 3.7 cm/yr in the precocious GH-deficient children but increased after the addition of GH to 7.4 cm during the first year of combination therapy. After 2 to 3 years of combination therapy, height predictions increased an average of 10 cm, compared with an increase of 2.8 cm in the precocious GH-sufficient group treated with gonadotropin releasing-hormone agonist alone. We conclude that combination treatment with gonadotropin releasing-hormone agonist and GH improves the height prognosis of children with coexistent true precocious puberty and GH deficiency, but falls short of achieving normal adult height potential.

Age Determination by Skeleton↗
PubMed1984

Ovulatory response, and plasma concentrations of luteinizing hormone and progesterone following administration of synthetic mammalian or chicken luteinizing hormone-releasing hormone relative to the first or second ovulation in the sequence of the domestic hen.

Experiments were conducted to investigate hypophyseal and follicular competency at two distinct stages of the hen's egg laying sequence: 1) 14 h prior to the first (C1) ovulation of a sequence (27 h following the previous ovulation); and 2) 14 h prior to the second (C2) ovulation of a sequence (13 h following the previous ovulation). When a single dose of mammalian luteinizing hormone-releasing hormone (mLHRH) or chicken luteinizing hormone-releasing hormone (cLHRH) was injected 14 h prior to a C1 ovulation, premature ovulation was induced in 19 of 20 hens. In contrast, ovulation was premature in only 1 of 20 hens when mLHRH or cLHRH was injected 14 h prior to a C2 ovulation. There was no difference between the two stages of the sequence in the amount of luteinizing hormone (LH) released for up to 60 min following a single i.v. injection of 20 micrograms mLHRH. However, only prior to a C1 ovulation did LH levels further increase to reach preovulatory concentrations. By contrast, progesterone (P4) concentrations were increased within the first 60 min to a lesser extent in hens injected prior to a C2 ovulation compared to a C1 ovulation. In C2-injected birds, P4 fell to levels that were not different from vehicle-injected controls by 45 to 60 min following injection, whereas P4 secretion was maintained in hens injected prior to a C1 ovulation. We suggest that the lack of sustained LH secretion following treatment with either species of LHRH 14 h prior to a C2 ovulation is related to follicular immaturity with respect to ability to produce and secrete P4. At the dosage administered, there was no difference in the ability of mLHRH compared to cLHRH to release LH at either stage of the sequence. Finally, two successive injections of mLHRH at 14 and 13 h prior to a C2 ovulation induced premature ovulation in 6 of 11 hens. It is suggested that LH, and possibly P4, exerts a priming effect on the largest preovulatory follicle to initiate fully potentiated P4 production and secretion.

Animals↗
PubMed1982

Luteinizing hormone-releasing hormone and thyrotropin-releasing hormone in human and bovine milk.

Two hypothalamic peptide hormones, luteinizing hormone-releasing hormone (LHRH) and thyrotropin-releasing hormone (TRH), have been isolated from human milk and bovine colostrum. Acidified methanolic extracts, prepared from human milk, bovine colostrum and rat hypothalami, as well as synthetic LHRH and TRH markers were subjected to high-pressure liquid chromatography (HPLC). The eluates were tested for the presence of LHRH and TRH by specific radioimmunoassays. It was found that milk extracts contain significant amounts of LHRH (3.9 - 11.8 ng/ml) and TRH (0.16 - 0.34 ng/ml), which comigrate with the corresponding marker hormones and with those of hypothalamic origin. The HPLC-purified LHRH from both human and bovine milk was bioactive in a dose-response manner similar to synthetic LHRH.

Animals↗
PubMed1987

In vivo release of dopamine, luteinizing hormone-releasing hormone and thyrotropin-releasing hormone in male rats bearing a prolactin-secreting tumor.

The present study was concerned with the effects of a transplantable prolactin-secreting pituitary tumor (7315b) on the hypothalamic release of dopamine, luteinizing hormone-releasing hormone (LHRH) and thyrotropin-releasing hormone (TRH) in gonadectomized, adrenalectomized male rats bearing subcutaneously a testosterone capsule and a corticosterone pellet. Similar male rats not inoculated with tumor served as controls. The rats were studied 3-4 weeks after tumor inoculation, while they were anesthetized with urethane. Compared to the controls, prolactin levels in the tumor-bearing rats had increased 70-fold, whereas the levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) decreased to 20 and 27%, respectively. In tumor-bearing rats, the secretion of dopamine into hypophysial stalk plasma increased from 2.3 to 4.9 ng/h (p less than 0.025), whereas that of LHRH decreased from 127 to 52 ph/h (p less than 0.005). Since the use of urethane anesthesia may change quantitatively and qualitatively the effects of hyperprolactinemia, it was decided to study these effects on the in vivo release of LHRH, dopamine and TRH in conscious rats by a push-pull perfusion of the median eminence-arcuate nucleus area. Using this technique, it was found that in tumor-bearing rats the secretion of LHRH decreased from 20.0 to 9.8 pg/15 min (p less than 0.005), whereas that of dopamine increased from 118 to 246 pg/15 min (p less than 0.025). The secretion of TRH was not altered by hyperprolactinemia (4.1 vs. 4.4 pg/15 min).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed2004

Interrelationships between hormones, behavior, and affect during adolescence: complex relationships exist between reproductive hormones, stress-related hormones, and the activity of neural systems that regulate behavioral affect. Comments on part III.

Adolescence is a period in life marked by change, encompassing physiological changes associated with pubertal development, changes in social status and the social stresses that an individual faces, and changes in behavioral affect regulation. The interactions between activity in the reproductive axis, the neural systems that regulate stress, hormones produced in response to stress, and neural systems governing behavioral affect regulation are complex and multifaceted. Although our understanding of these interactions remains rudimentary, we do know that stress can suppress activity of the reproductive axis, that reproductive hormones can modulate the activity of neural systems that govern the body's responses to stress, that both reproductive function and stress responsiveness can be altered in depressed individuals, and that the function of some of the key neural systems regulating behavioral affect (i.e., serotonergic, noradrenergic, dopaminergic systems) are modulated by both gonadal steroid hormones and adrenal steroid hormones. This summary reviews the central interactions discussed in this session on the interrelationships between hormones, behavior, and affect during adolescence and identifies key topics that require further investigation in order to understand the role that pubertal changes in reproductive function, interacting with increased exposure to life stresses, play in modulating behavioral affect regulation during the adolescent period.

Adolescent↗
PubMed1995

Lys91 and His90 of the alpha-subunit are crucial for receptor binding and hormone action of follicle-stimulating hormone (FSH) and play hormone-specific roles in FSH and human chorionic gonadotropin.

Glycoprotein hormones, FSH, LH, CG, and TSH, consist of a common alpha-subunit and a hormone-specific beta-subunit. Both subunits are thought to interact with the hormone receptors. Although several C-terminal residues of hCG alpha are known to contact the LH/CG receptor, little is known about the roles of individual C-terminal residues of FSH alpha. In this report, substitutions of various amino acids for the penultimate Lys91 and the upstream His90 of the alpha-subunit demonstrate that these two residues of FSH alpha are important for high affinity receptor binding and hormone action to induce cAMP production. In contrast, the same residues of hCG alpha are more important for cAMP induction than for high affinity receptor binding. Some substitutions significantly improved receptor binding of FSH and hCG, whereas others were detrimental. Some had the same effect on both hormones, and others impacted differently. Particularly, the substitution of Val for alpha Lys91 resulted in an improved receptor binding of and a loss of cAMP induction by FSH and hCG. On the other hand, the substitution of Arg or Pro for alpha His90 abolished receptor binding of FSH, but not of hCG. These results allowed us to generate an antagonist to FSH. Our results indicate that alpha His90 and alpha Lys91 play roles in receptor binding and cAMP induction of FSH and hCG in strikingly different ways. They will be useful to elucidate the underlying mechanisms for the interaction of FSH and hCG with their complementary receptors as well as for receptor activation.

Animals↗
PubMed1997

Thyroid hormone and glucocorticoid regulation of pituitary growth hormone-releasing hormone receptor gene expression.

The GH-releasing hormone receptor (GHRH-R) is a critical link between hypothalamic GH-releasing hormone (GHRH) and pituitary GH secretion. However, the factors that regulate GHRH-R are not well understood. Despite the importance of thyroid hormone and glucocorticoids in influencing the GH axis in vivo, it is not known whether these hormones act directly at the pituitary to regulate expression of GHRH-R. We tested the effects of T3 and hydrocortisone on GHRH-R gene expression in primary pituitary cell cultures of adult male rats. Pituitary cells were treated for 24h with increasing concentrations of T3 (0.06-60 nM) or hydrocortisone (2.8 nM-2.8 microM). GHRH-R mRNA levels were assessed by ribonuclease protection assay. T3 caused a striking dose-dependent increase in GHRH-R mRNA, reaching levels 5.1 +/- 0.5 fold over controls (P < 0.001). Hydrocortisone also stimulated a marked dose-dependent increase in GHRH-R mRNA, reaching levels 5.6 +/- 0.7 fold over controls (P < 0.001). Combined treatment with both hormones did not cause further augmentation of GHRH-R mRNA levels. These data indicate that T3 and hydrocortisone act directly at the pituitary as potent regulators of GHRH-R gene expression.

Animals↗
PubMed1983

Effects of thyrotropin-releasing hormone and a thyrotropin releasing hormone analog on growth and selected plasma hormones in lambs.

An 8-wk growth trial was conducted to assess the effects of continuous infusion of thyrotropin-releasing hormone (TRH) and an active TRH analog less than Aad-His-Pro-NH2 (the less than Aad is L-pyro-alpha-aminoadipic acid) on growth trial performance, carcass composition and hormone profiles of growing lambs. Both drugs were infused at 600 micrograms X lamb -1 X d -1 with 16 lambs/treatment. Both TRH and less than Aad-His-Pro-NH2 decreased average daily gain (ADG; P less than .01) and increased feed conversion (FC; P less than .01) compared with saline infused controls. Average daily feed intake was not altered. Carcasses of lambs given TRH or less than Aad-His-Pro-NH2 contained fewer kilograms of moisture (P less than .05) and appeared to contain fewer kilograms of protein. Thyrotropin-releasing hormone and less than Aad-His-Pro-NH2 increased thyroid gland weights (P less than .05), but pituitary gland weights were not different. Plasma thyrotropin (TSH) concentrations were increased by both drugs compared with control lambs, peaking at 4 to 7 d after initiating infusion. However, by 14 d, TSH concentrations returned to control levels. Triiodothyronine (T3) and thyroxine (T4) were elevated by both drugs over the entire 8-wk trial, with peak levels reached at 10 d and maintained for the duration of the study. Both TRH and less than Aad-His-Pro-NH2 increased prolactin over the entire period. Growth hormone levels were not altered by either drug. The effects of less than Aad-His-Pro-NH2 infusion on growth trial performance, carcass composition and hormone profiles of growing lambs were very similar to TRH. The negative effects of TRH and less than Aad-His-Pro-NH2 infusion on ADG, FC and carcass protein appear to be the result of elevated T3 and T4 levels.

Animals↗