首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献，搜索用时 31 毫秒
1.
The pituitary gland, occupying a central position in the hypothalamo-pituitary thyroidal axis, produces thyrotropin (TSH), which is known to stimulate the thyroid gland to synthetize and release its products, thyroid hormones. TSH is produced by a specific cell population in the pituitary, the so-called thyrotropes. Their secretory activity is controlled by the hypothalamus, releasing both stimulatory and inhibitory factors that reach the pituitary through a portal system of blood vessels. Based on early experiments in mammals, thyrotropin-releasing hormone (TRH) is generally mentioned as the main stimulator of the thyrotropes. During the past few decades, it has become clear that the hypophysiotropic function of the hypothalamus is more complex, with different hormonal axes interacting with each other. In the chicken, it was found that not only TRH, but also corticotropin-releasing hormone (CRH), the main stimulator of corticotropin release, is a potent stimulator of TSH secretion. Somatostatin (SRIH), a hypothalamic factor known for its inhibitory effect on growth hormone secretion, was demonstrated to blunt the TSH response to TRH and CRH. In this review we summarize the latest studies concerning the "interaxial" hypothalamic control of TSH release in the chicken, with a special emphasis on the molecular components of these control mechanisms. It remains to be demonstrated if these findings could also be extrapolated to other species or classes of vertebrates.  相似文献   

2.
Thyrotropin (TSH) responses were determined in eight healthy male beagle dogs after a single administration of thyrotropin-releasing hormone (TRH) and the combined administration of four hypothalamic releasing hormones, i.e., corticotropin-releasing hormone, growth hormone-releasing hormone, gonadotropin-releasing hormone, and TRH. In both tests, TRH was administered in a dose of 10 μg/kg. Basal TSH concentrations ranged form 0.07 to 0.27 μg/1(mean ± SE, 0.14 ± 0.02 μg/1). The administration of TRH, alone or in the combined test, resulted in a prompt and significant increase in TSH with mean (±SE) plasma TSH peaks of 1.26 ± 0.22 μg/1 at 10 min and 0.85 ± 0.17 μg/1 at 30 min, respectively. The area under the curve (0–120 min) was significantly lower in the combined test than in the single TRH test, whereas the increments were not significantly different. It is concluded that measurements of TSH responses to TRH alone and in combination with other releasing hormones can be used for the assessment of pituitary thyrotropic cell function. In the combined test, the TSH response is slightly lower than that in the single test.  相似文献   

3.
Serum concentrations of thyrotropin (TSH), prolactin, thyroxine, and 3,5,3'-triiodothyronine in 15 euthyroid dogs and 5 thyroidectomized and propylthiouracil-treated dogs after thyrotropin-releasing hormone (TRH) administration were measured. Although thyroidectomized and propylthiouracil-treated dogs had higher (P less than 0.01) base-line concentrations of TSH in serum than did euthyroid dogs, concentrations of TSH after TRH administration varied at 7.5, 15, and 30 minutes with 14 of 45 samples obtained from healthy dogs having lower TSH concentrations than before TRH challenge. Similarly, concentrations of 3,5,3'-triiodothyronine in the serum of euthyroid dogs 4 hours after TRH administration were similar (P less than 0.05) to concentrations before TRH challenge. Although the mean concentration of thyroxine in serum was elevated (P less than 0.05) 4 hours after administration of TRH to euthyroid animals, as compared with base-line levels, the individual response was variable with concentrations not changing or decreasing in 4 dogs. Therefore, the TRH challenge test as performed in the current investigation was of limited value in evaluating canine pituitary gland function. Although mean concentrations of TSH in serum were higher (P less than 0.05) in euthyroid dogs after TRH administration, the response was too variable among individual animals for accurate evaluation of pituitary gland function. Concentrations of prolactin in the sera of dogs after TRH administration, confirmed previous reports that exogenously administered TRH results in prolactin release from the canine pituitary and indicated that the TRH used was biologically potent.  相似文献   

4.
From case studies in humans it is known that primary hypothyroidism (PH) may be associated with morphological and functional changes of the pituitary. There is no insight into the time scale of these changes. In this study, seven beagle dogs were followed up for 3 years after the induction of primary hypothyroidism. Three of these dogs were followed up for another 1.5 years while receiving l-thyroxine. Adenohypophyseal function was investigated at 2-month intervals with the combined intravenous injection of CRH, GHRH, GnRH, and TRH, and measurement of the plasma concentrations of ACTH, GH, LH, PRL, and TSH. In addition, after 2 years of hypothyroidism a single TRH-stimulation test and a somatostatin test were performed, with measurements of the same pituitary hormones. Every 6 months the pituitary gland was visualized by computed tomography (CT). Induction of PH led to high plasma TSH concentrations for a few months, where after concentrations gradually declined to values no longer significantly different from pre-PH values. A blunted response to stimulation of TSH release preceded this decline. Basal plasma GH concentrations increased during PH and there was a paradoxical hyperresponsiveness to TRH stimulation. Basal GH concentrations remained elevated and returned only to low values during l-thyroxine treatment. Basal PRL concentrations decreased significantly during PH and normalized after several months of l-thyroxine treatment. The pituitary gland became enlarged in all dogs. Histomorphology and immunohistochemical studies in 4 dogs, after 3 years of PH, revealed thyrotroph hyperplasia, large vacuolated thyroid deficiency cells, and decreased numbers of mammotrophs. Several cells stained for both GH and TSH. In conclusion, with time PH led to a loss of the TSH response to low T4 concentrations, hypersecretion of GH, and hyposecretion of PRL. The enlarged pituitaries were characterized by thyrotroph hyperplasia, large vacuolated thyroid deficiency cells, and double-staining cells, which are indicative of transdifferentiation.  相似文献   

5.
Plasma concentrations of thyroxine (T4) and triiodothyronine (T3) were profoundly depressed both in chick embryos and growing chickens after methimazole (MMI) treatment. There was no response of T4 and T3 levels to TRH or TSH injections in the MMI group, either in embryos or growing chickens.

Peroxidase activity measured in the thyroid gland was significantly higher in embryos and growing chickens treated with MMI. However, neither TRH nor TSH affected this activity 2 hr after injection in either control or the MMI-treated group.

Hepatic 5′-monodeiodinase activity was significantly stimulated in the MMI-treated groups of embryos and growing chickens but only when additional sulphydryl groups (DTT) were provided. In embryos, monodeiodination activity 2 hr after TSH injection was not significantly different from control values for either DTT-stimulated or unstimulated conditions within the control and MMI-infused groups. However, in both control and MMI-treated embryos monodeiodination activity significantly increased 2 hr after TRH injection. In the growing chickens, monodeiodination activity 2 hr after TRH or TSH injection was not significantly different from control values in either stimulated or unstimulated conditions of each group.  相似文献   


6.
Previously it has been shown that androgen suppresses transportation-induced increases in plasma adrenocorticotropic hormone (ACTH), possibly by suppressing the secretion of corticotrophin releasing hormone (CRH) or arginine vasopressin (AVP) from the hypothalamus, or secretion of ACTH from the pituitary gland. The aim of the present study was to examine androgen target sites in the caprine diencephalon and pituitary gland using immunohistochemical methods. The androgen receptor (AR) was expressed strongly in the bed nucleus of the stria terminalis, the medial preoptic area, the arcuate nucleus, the ventromedial hypothalamic nucleus and the suprachiasmatic nucleus in the diencephalon. Between 8% and 11% of CRH and AVP neurons in the paraventricular hypothalamic nucleus (PVN) expressed AR. In the pituitary gland, 7.1% of corticotrophs expressed AR. The results are consistent with the proposal that androgen acts directly and indirectly on CRH and/or AVP neurons in the PVN. The possibility of a direct action of androgen on the corticotrophs in the pituitary gland was also considered.  相似文献   

7.
In order to clarify the functional relationship between thyroid, adrenal and gonadal hormones, hypothyroidism was induced by administration of thiuoracil in adult male and female rats, and the effects of hypothyroidism on the adrenal and the gonadal axes were investigated in the present study. 1. The functional relationship between thyroid and adrenal hormones: Adrenal weights and corticosterone were lowered, whereas the secretion of ACTH, corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP) increased in hypothyroid rats compared to euthyroid rats. These results indicate that hypothyroidism causes adrenal dysfunction directly and results in hypersecretion of CRH and AVP from the hypothalamus. 2. The functional relationship between thyroid and gonadal hormones: The pituitary response to LHRH was lowered, whereas the testicular response to hCG was not changed in hypothyroid rats. Hypothyroidism suppressed copulatory behavior in male rats. These results suggest that hypothyroidism probably causes dysfunction in gonadal axis at the hypothalamic-pituitary level in male rats. In adult female rats, hypothyroidism inhibited the follicular development accompanied estradiol secretion, whereas plasma concentrations of progesterone and prolactin (PRL) increased in hypothyroid female rats. Hypothyroidism significantly increased the pituitary content of vasoactive intestinal peptide (VIP) though it did not affect dopamine synthesis. These results suggest that hypothyroidism increases pituitary content of VIP and this increased level of VIP likely affects PRL secretion in a paracrine or autocrine manner. In female rats, inhibition of gonadal function in hypothyroid rats mediated by hyperprolactinemia in addition to hypersecretion of endogenous CRH.  相似文献   

8.
It has previously been demonstrated that naloxone and morphine modify the adrenocortical and pituitary responses of sheep to stress. Since CRH acts within the brain to co-ordinate the stress response, the present experiment was conducted to determine whether morphine has similar effects in sheep given oCRH centrally. Plasma concentrations of cortisol, prolactin and growth hormone were measured in blood samples collected at 10 min intervals from sheep (N = 5) over a 3-hr period. Intravenous injections of saline vehicle or morphine sulphate (0.4 mg/kg) were given after 40 min and intracerebroventricular injections of oCRH (0, 5 or 20 micrograms) were administered after 60 min. Sustained, dose-related, increases in cortisol were induced by oCRH and, in agreement with findings in stressed sheep, these responses were reduced by pretreatment with morphine. Prolactin levels appeared to increase after morphine but oCRH, on its own, did not increase prolactin secretion in this study. There was no change in growth hormone concentrations after oCRH whereas morphine transiently stimulated release.  相似文献   

9.
Background: Glucocorticoids(GCs) are involved in the control of appetite in birds and mammals. The effect of GCs on feed intake in birds depends on their dietary energy level. But the regulation mechanism of GCs on appetite is still unclear in chickens facing to different energy level. An experiment was conducted to investigate the effect of dexamethasone(DEX) on hypothalamic expression of appetite-related peptides in chickens fed high/low fat diet and under fasting/feeding condition.Results: An interaction between DEX injection and dietary energy level was found on hypothalamic corticotropinreleasing hormone(CRH) gene expression in fasted chickens(P 0.05). The chickens, given a DEX injection and a low fat diet treatment, had the highest CRH m RNA levels than any of the fasted chickens given treatments(P 0.05).Under fasting conditions, the DEX treatment significantly increased hypothalamic neuropeptide Y(NPY) and GC receptors m RNA levels(P 0.05). Under re-feeding conditions, DEX treatment significantly decreased hypothalamic expression levels of NPY and agouti-related peptide(Ag RP) but significantly increased the level of hypothalamic CRH expression(P 0.05).Conclusion: A regulatory network formed by NPY, Ag RP and CRH is associated with the appetite-control by GCs.The result suggests that the regulation of GCs on orexigenic neuropeptides expression is dependent at least partially on dietary energy level and feeding state.  相似文献   

10.
The effects of propylthiouracil (PTU)-induced thyroid hormone imbalance on GH, TSH and IGF-I status in cattle were examined. In the first study, four crossbred steers (avg wt 350 kg) were fed a diet dressed with PTU (0, 1, 2 or 4 mg/kg/d BW) in a Latin square design with four 35-d periods. On day 29 in each period, steers were challenged with an intrajugular bolus of thyrotropin releasing hormone (TRH, 1.0 μg/kg). Blood samples were obtained to assess the change in plasma GH and TSH as affected by PTU. Plasma IGF-I was measured from blood samples obtained before and after (every 6 hr for 24 hr) intramuscular injection of bovine GH (0.1 mg/kg, day 31). Doses of 1 and 2 mg/kg PTU increased plasma T4 (P<.01). At 4 mg/kg, PTU depressed T4 concentrations to 30% of control (P<.01). Plasma T3 linearly decreased with increasing doses of PTU (P<.01). Plasma TSH increased when PTU was fed at 4 mg/kg (P<.05) while the TSH response to TRH declined with increasing PTU (P<.02). Neither basal nor TRH-stimulated plasma concentration of GH was affected by PTU; the IGF-I response to GH tended to increase at the 1 and 2 mg/kg PTU (P<.01). In a second study 24 crossbred steers were fed PTU (1.5 mg/kg) for 119 d in a 2 × 2 factorial design with implantation of the steroid growth effector, Synovex-S (200 mg progesterone + 20 mg estradiol), as the other main effect. Basal plasma GH and IGF-I were not affected by PTU treatment. Synovex increased plasma concentration (P<.01) of IGF-I without an effect on plasma GH. The data suggest that mild changes in thyroid status associated with PTU affects regulation of T3, T4 and TSH more than GH or IGF-I in steers.  相似文献   

11.
1. The effects of daily injections of corticosterone (1 or 5 mg/bird) on growth, fat deposition, liver lipid and plasma concentrations of uric acid, glucose, insulin and growth hormone were studied using genetically selected lines of fat (FL) and lean (LL) chickens. 2. Both doses of corticosterone depressed body weight gain and increased the liver lipid and the abdominal fat to the same extent in both lines. 3. In both lines, corticosterone caused a dose-dependent increase in the plasma concentrations of uric acid, glucose and insulin in the fasted and refed states. 4. In untreated birds, plasma concentrations of growth hormone (GH) were slightly higher in FL than in LL chickens and slightly decreased during refeeding. The response was not modified by injection of 1 mg corticosterone. Injections of 5 mg decreased plasma GH in both lines in the fasting state and in LL chickens during refeeding. In contrast, the same dose increased GH in FL chickens during refeeding. This contradiction remains unexplained. 5. The results suggest that corticosterone sensitivity is not involved in difference of fattening between FL and LL chickens.  相似文献   

12.
Pit-1 is a pituitary-specific POU-domain DNA binding factor, which binds to and trans-activates promoters of growth hormone- (GH), prolactin- (PRL) and thyroid stimulating hormone-beta- (TSHbeta) encoding genes. Thyrotropin-releasing hormone (TRH) is located in the hypothalamus and stimulates TSH, GH and PRL release from the pituitary gland. In the present study, we successfully used the cell aggregate culture system for chicken pituitary cells to study the effect of TRH administration on the ggPit-l* (chicken Pit-1), GH and TSHbeta mRNA expression in vitro. In pituitary cell aggregates of 11-day-old male broiler chicks the ggPit-l * mRNA expression was significantly increased following TRH administration, indicating that the stimulatory effects of TRH on several pituitary hormones are mediated via its effect on the ggPit-l* gene expression. Therefore, a semiquantitative RT-PCR method was used to detect possible changes in GH and TSHbeta mRNA levels. TRH affected both the GH and TSHbeta mRNA levels. The results of this in vitro study reveal that ggPit-1 * has a role in mediating the stimulatory effects of TRH on pituitary hormones like GH and TSHbeta in the chicken pituitary.  相似文献   

13.
The control of growth is a complex mechanism regulated by several metabolic hormones including growth hormone (GH) and thyroid hormones. In avian species, as well as in mammals, GH secretion is regulated by hypothalamic hypophysiotropic hormones. Since thyrotropin-releasing hormone (TRH) and growth hormone-releasing factor (GRF) are potent GH secretagogues in poultry, we were interested in determining the influence of daily intravenous administration of either peptide or both simultaneously on circulating GH and IGF-I concentrations and whether an improvement in growth rate or efficiency would be obtained.

Male broiler chicks were injected once daily for a period of 21 days with either GRF (10 μg/kg), TRH (1 μg/kg) or both GRF and TRH (10 and 1 μg/kg respectively) between four and seven weeks of age. On the last day of the experiment, following intravenous injection of TRH, GRF or a combination of GRF and TRH, plasma GH levels were significantly (P<.05) increased to a similar extent in control chicks and in those which had received daily peptide injections for the previous 21 days. Circulating GH levels between 10 and 90 min post-injection were significantly (P<.05) greater and more than additive than GH levels in chicks injected with both GRF and TRH when compared to those injected with either peptide alone. Mean plasma T3 concentrations during that same time period were significantly elevated (P<.05) above saline-injected control chick levels in birds treated with TRH or GRF and TRH respectively, regardless of whether the chicks had received peptide injections for the previous 21 days. There was no evidence of pituitary refractoriness to chronic administration of either TRH or GRF injection in terms of growth or thyroid hormone secretion.

Despite the large elevation in GH concentration each day, growth rate, feed efficiency and circulating IGF-I concentrations were not enhanced. Thus the quantity or secretory pattern of GH secretion induced by TRH or GRF administration was not sufficient to increase plasma IGF-I concentration or growth.  相似文献   


14.
A combined anterior pituitary (CAP) function test was assessed in eight healthy male beagle dogs. The CAP test consisted of sequential 30-second intravenous administrations of four hypothalamic releasing hormones in the following order and doses: 1 μg of corticotropin-releasing hormone (CRH)/kg, 1 μg of growth hormone-releasing hormone (GHRH)/kg, 10 μg of gonadotropinreleasing hormone (GnRH)/kg, and 10 μg of thyrotropin-releasing hormone (TRH)/kg. Plasma samples were assayed for adrenocorticotropin, cortisol, GH, luteinizing hormone (LH), and prolactin (PRL) at multiple times for 120 min after injection. Each releasing hormone was also administered separately in the same dose to the same eight dogs in order to investigate any interactions between the releasing hormones in the combined function test.Compared with separate administration, the combined administration of these four hypothalamic releasing hormones caused no apparent inhibition or synergism with respect to the responses to CRH, GHRH, and TRH. The combined administration of these four hypothalamic releasing hormones caused a 50% attenuation in LH response compared with the LH response to single GnRH administration. The side effects of the combined test were confined to restlessness and nausea in three dogs, which disappeared within minutes after the administration of the releasing hormones. It is concluded that with the rapid sequential administration of four hypothalamic releasing hormones (CRH, GHRH, GnRH, and TRH), the adenohypophyseal responses are similar to those occurring with the single administration of these secretagogues, with the exception of the LH response, which is lower in the CAP test than after single GnRH administration.  相似文献   

15.
Studies were conducted to determine the specificity and cause of altered pituitary hormone secretion when ewes ingest endophyte-infected (Acremonium coenophialum) GI-307 tall fescue (toxic fescue). Plasma concentrations of prolactin (PRL) but not growth hormone (GH) or thyroid stimulating hormone (TSH) in ewes grazing toxic fescue were significantly lower (P < .01) than concentrations measured in ewes grazing orchardgrass (OG). Comparing hormone secretory responses of ewes grazing each grasstype, ewes on toxic fescue released less PRL following thyrotropin releasing hormone (TRH) challenge than ewes on OG. TSH responses to TRH were not affected by grasstype. At this dose of TRH, GH secretion was not significantly affected in either group of ewes. In a separate study, dopamine hydrochloride (DA) was infused into control ewes to define the effect of a pure dopamine agonist on basal and TRH-stimulated secretion of PRL, GH and TSH. DA depressed both basal and TRH-stimulated secretion of PRL without affecting the basal concentrations or responses of GH or TSH. Based on the assumption that the active agent in toxic fescue responsible for the observed hypoprolactinemia was a dopaminergic agonist, haloperidol (HAL), a DA receptor blocking drug, was administered to ewes grazing toxic fescue or OG. HAL evoked significant PRL secretion unaccompanied by any GH or TSH effect in both toxic fescue and OG ewes. Administration of HAL resulted in a gradual increase over 4 hr in PRL in toxic fescue ewes and prolonged the duration of the PRL response to TRH. No differences in circulating plasma concentrations of DA, epinephrine or norepinephrine were measured in ewes on troxic fescue or OG.

Alterations in pituitary hormone secretion due to toxic factors in fescue were confined to PRL. Hormone secretory responses to TRH and HAL suggest that the effects on PRL are mediated through dopamine-like activity in toxic fescue.  相似文献   


16.
Pit-1 is a pituitary-specific POU-domain DNA binding factor, which binds to and trans-activates promoters of growth hormone- (GH), prolactin- (PRL) and thyroid stimulating hormone beta- (TSHbeta) encoding genes. Pit-1 has been identified in several mammalian and avian species. Thyrotropin-releasing hormone (TRH) is located in the hypothalamus and it stimulates TSH, GH and PRL release from the pituitary gland. In the present study, we successfully developed a competitive RT-PCR for the detection of Pit-1 expression in the chicken pituitary, that was sensitive enough to detect picogram levels of Pit-1 mRNA. Applying this method, the effect of TRH injections on Pit-1 mRNA expression was determined in the pituitary of chick embryos and growing chicks. In both 18-day-old embryos and 10-day-old male chicks the Pit-1 mRNA expression was significantly increased following TRH injection, thereby indicating that the stimulatory effects of TRH on several pituitary hormones is mediated via its effect on Pit-1 expression. Therefore, a semi-quantitative RT-PCR method was used to detect possible changes in GH levels. TRH affected the GH mRNA levels at both developmental stages. These results, combined with the data on Pit-1 mRNA expression, indicate that Pit-1 has a role in mediating the stimulatory effects of TRH on pituitary hormones like GH.  相似文献   

17.
Supplemental dietary fat provides excess fatty acids (FA), which can alter circulating concentrations of several hormones. To test the effects of fatty acid isomer type and possible sites of regulation, we abomasally infused fat mixtures high in cis-C18:1 FA (iTRS) or no infusion (NI) and performed intravenous arginine (ARG) and intramuscular thyrotropin-releasing hormone (TRH) challenges. The experimental design was a replicated 3 × 3 Latin square. Challenges were conducted on Days 10 (ARG) and 12 (TRH) after initiation of fat infusion on each of three 4-wk experimental periods. Plasma concentrations of IGF-I were lower (P < 0.01) when cows received iCIS or iTRS compared with NI. Plasma insulin concentrations increased with ARG but responses were not affected by FA. Plasma growth hormone (GH) was unchanged after ARG. Peak plasma GH and thyroid-stimulating hormone (TSH) responses to TRH were blunted (P < 0.05 and P < 0.1, respectively), whereas thyroxine (T4) and triiodothyronine (T3) responses were augmented post-TRH (P < 0.01) when cows received either FA isomer. Prolactin responses to TRH were not different between infusion treatments, although basal plasma concentrations before TRH were higher in cows infused with iTRS (P < 0.05). To focus on fat regulation of the thyroid axis, we tested directly in vitro the ability of fatty acids dissolved with sodium taurocholate to affect Type-I 5'-deiodinase (5'D) activity in bovine liver homogenates. Homogenate 5'D was not affected by C2:0---C10:0 fatty acids, but decreased linearly (P < 0.01) with increasing concentrations of C12:0---C16:0 and C18:1 isomers. CisC18:1 decreased 5′D more than the trans-isomer (P < 0.01), the difference was only apparent at concentrations greater than 0.25 mM. The data suggest that various aspects of pituitary hormone regulation are differentially affected by FA composition. Fatty acid infusion may accentuate end organ responses in the thyroid axis and decrease IGF-I in the somatotropic axis. The data also suggest that FA isomer may alter patterns of extrathyroidal generation of thyroid hormones via direct influences on 5′D.  相似文献   

18.
Six insulin-sensitive and 6 insulin-insensitive mares were used in a replicated 3 by 3 Latin square design to determine the pituitary hormonal responses (compared with vehicle) to sulpiride and thyrotropin-releasing hormone (TRH), 2 compounds commonly used to diagnose pituitary pars intermedia dysfunction (PPID) in horses. Mares were classified as insulin sensitive or insensitive by their previous glucose responses to direct injection of human recombinant insulin. Treatment days were February 25, 2012, and March 10 and 24, 2012. Treatments were sulpiride (racemic mixture, 0.01 mg/kg BW), TRH (0.002 mg/kg BW), and vehicle (saline, 0.01 mL/kg BW) administered intravenously. Blood samples were collected via jugular catheters at −10, 0, 5, 10, 20, 30, 45, 60, 90, and 120 min relative to treatment injection. Plasma ACTH concentrations were variable and were not affected by treatment or insulin sensitivity category. Plasma melanocyte-stimulating hormone (MSH) concentrations responded (P < 0.01) to both sulpiride and TRH injection and were greater (P < 0.05) in insulin-insensitive mares than in sensitive mares. Plasma prolactin concentrations responded (P < 0.01) to both sulpiride and TRH injection, and the response was greater (P < 0.05) for sulpiride; no effect of insulin sensitivity was observed. Plasma thyroid-stimulating hormone (TSH) concentrations responded (P < 0.01) to TRH injection only and were higher (P < 0.05) in insulin-sensitive mares in almost all time periods. Plasma LH and FSH concentrations varied with time (P < 0.05), particularly in the first week of the experiment, but were not affected by treatment or insulin sensitivity category. Plasma GH concentrations were affected (P < 0.05) only by day of treatment. The greater MSH responses to sulpiride and TRH in insulin-insensitive mares were similar to, but not as exaggerated as, those observed by others for PPID horses. In addition, the reduced TSH concentrations in insulin-insensitive mares are consistent with our previous observation of elevated plasma triiodothyronine concentrations in hyperleptinemic horses (later shown to be insulin insensitive as well).  相似文献   

19.
Stressors generally induce a depression of the hypothalamus-pituitary-testis (HPT) system, mediated by the activated hypothalamus-pituitary-adrenocortical (HPA) system, resulting in a fall in plasma luteinising hormone (LH) and testosterone levels. Hypothalamic gonadotrophin-releasing hormone (GnRH) secretion may be suppressed by endogenous opioid peptides (EOP) and/or corticosteroids. The latter dramatically enhance the negative feedback effects of testosterone on both the hypothalamus and pituitary. Pituitary gonadotrophin secretion may be reduced by adrenocorticotrophic hormone or by EOP of hypothalamic or pituitary origin. Decreases in plasma concentrations of testosterone, independent of gonadotrophins, can be induced by corticosteroids. These hormones might reduce the number of Leydig-cell LH-receptors or occupation of LH-receptors. Testicular steroidogenesis may also be inhibited by pro-opiomelanocortin-derived (opioid) peptides secreted by the Leydig cells. There are some indications of increases in LH and testosterone during acute stress and, in dominant male animals, during the stress of social conflict. The latter finding indicates a difference in stress response between dominant and subordinate males. In subordinate males, decreased feedback sensitivity may allow hypersecretion throughout the HPA system. As a result, corticotrophin releasing hormone may induce the release of EOP from the hypothalamus, which inhibit the HPT axis. This inhibition may be enhanced by a corticosteroid-induced decrease in testosterone feedback.  相似文献   

20.
The effects of estrogen and fasting on hepatic metabolism were studied by an arteriovenous difference technique in six multicatheterized ewes. In each experiment samples were collected during fed and 3- and 5-day fasted states before, and 10 to 17 days after the animals had been implanted with 550 mg of estradiol-17 beta. The implants elevated plasma estradiol five- to seven-fold. Plasma concentrations of insulin and triglyceride (TG) were increased (P less than 0.01) by 131% and 62% respectively by estradiol in fed sheep. Concurrent circulating concentrations of glucose, glycerol, free fatty acids, and beta-hydroxybutyrate were unaffected. During fasting estradiol elevated circulating concentrations of beta-hydroxybutyrate slightly, while levels of other metabolites and insulin were not different from fasted controls. In fed animals estradiol had no effect on the net hepatic uptake (NHU) of TG or glycerol but during fasting estradiol reduced the NHU of TG and glycerol by 47% and 31% (P less than 0.01) respectively. In addition, estradiol reduced the net hepatic production of beta-hydroxybutyrate in fed, but not in fasted animals. Net hepatic exchanges of glucose, or FFA were not affected by estradiol in either the fed or fasted state. Fasting increased the NHU of TG (P less than 0.05) and glycerol (P less than 0.01). The results of this study suggest that estradiol, at physiological concentrations, has lipotropic and anti-ketogenic effects on the ruminant liver. However, the anti-ketogenic effect is not apparent in fasted animals. Secondly, it appears that the hepatic lipidosis which often occurs in ruminants during negative energy balance is due largely to an increase in the NHU of circulating TG.  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号