Kinetics of LRH-induced LH-release in vivo: influence of LRH pre-treatment

1982 ◽  
Vol 99 (2) ◽  
pp. 195-199 ◽  
Author(s):  
T. R. Koiter ◽  
N. Pols-Valkhof ◽  
G. A. Schuiling
Keyword(s):  
Priming Effect ◽  
Compartment Model ◽  
Secretion Rate ◽  
Ovx Rats ◽  
Lh Release ◽  
The Mean ◽  
Pre Treatment ◽  
Lh Secretion ◽  
Secretion Rates

Abstract. The influence of an LRH injection (50 ng/ 100 g b.w.) on the LH-response to a second, equally large LRH injection or a constant rate infusion of LRH (104 ng/h), administered 1 h later, was studied in phenobarbitone-anaesthetized, oil- or oestradiol benzoate (OeB)-treated rats ovariectomized (OVX) 5 weeks earlier. From the plasma LH concentration the mean maximal LH secretion rates, as well as the amounts of LH secreted, were calculated on the basis of a one-compartment model, proceeding from a half-life of LH of 15 min. In both the oil- and the OeB-treated animals, not only the mean maximal LH secretion rate, but also the amount of LH secreted during the first hour following the injection, was significantly higher after the second LRH injection than after the first one (LRH self-priming effect). Infusion of LRH in LRH-primed OVX rats revealed that the LH secretion accelerates immediately after the start of the infusion and this acceleration lasts about 1 h. In the saline-injected controls, on the other hand, the LH secretion, although elevated, remains constant during the first 30 min of LRH infusion and accelerates only thereafter during about 1 h. Yet, maximal LH secretion rates are not statistically different between the LRH-primed oil- or OeB-treated OVX rats and their respective saline-injected controls. It is concluded that the self-priming effect of LRH does not lead to an increase of the ultimate maximal LH secretion rate. Rather, during priming the conditions necessary for immediate acceleration of the LH secretion rate are established, and priming thus causes a shift in time, that is, an advancement, of the LH-response to a subsequent LRH stimulus.

scholarly journals Ovarian stimulation with FSH reduces phosphorylation of gonadotrope progesterone receptor and LH secretion in the rat

Reproduction ◽  
2009 ◽  
Vol 137 (1) ◽  
pp. 151-159 ◽  
Author(s):  
Ana Gordon ◽  
José C Garrido-Gracia ◽  
Rafaela Aguilar ◽  
Silvia Guil-Luna ◽  
Yolanda Millán ◽  
...  
Keyword(s):  
Progesterone Receptor ◽  
Ovarian Stimulation ◽  
Inhibitory Effect ◽  
Ovx Rats ◽  
Formalin Fixed Paraffin ◽  
Formalin Fixed Paraffin Embedded ◽  
Experimental Approaches ◽  
Lh Release ◽  
Lh Secretion

Administration of human FSH (hFSH) to cyclic rats during the dioestrous phase attenuates progesterone receptor (PR)-dependent events of the preovulatory LH surge in pro-oestrus. The increased bioactivity of the putative ovarian gonadotropin surge inhibiting/attenuating factor induced by hFSH treatment is not associated with a decrease in PR protein expression, and the possibility of its association at a PR posttranslational effect has been raised. The present experiments aimed to analyse PR phosphorylation status in the gonadotrope of rats with impaired LH secretion induced byin vivohFSH injection. Two experimental approaches were used. First, incubated pro-oestrous pituitaries from hFSH-injected cycling and oestrogen-treated ovariectomized (OVX) rats were used to analyze the effect of calyculin, an inhibitor of intracellular phosphatases, on PR-dependent LH release, which was measured in the incubation medium by RIA. Second, pituitaries taken from hFSH-injected intact cycling and OVX rats and later incubated with P or GNRH1 were used to assess the phosphorylation rate of gonadotrope. The latter was analysed in formalin-fixed, paraffin-embedded tissue sections by immunohistochemistry using a MAB that recognizes the phosphorylated (p) form of PR at Ser294. Calyculin reduced the ovary-mediated inhibition of hFSH in GNRH1-stimulated LH secretion. In addition, the immunohistochemical expression of pSer294 PR was significantly reduced after ovarian stimulation with hFSH in pituitaries from pro-oestrous rats incubated with P or GNRH1. Altogether, these results suggested that the ovarian-dependent inhibitory effect of FSH injection on the preovulatory LH secretion in the rat may involve an increase in dephosphorylation of PR.

Short-term kinetics of LRH-induced LH-release in the long-term ovariectomized rat

1982 ◽  
Vol 99 (2) ◽  
pp. 187-194 ◽  
Author(s):  
T. R. Koiter ◽  
N. Pols-Valkhof ◽  
G. A. Schuiling
Keyword(s):  
Luteinizing Hormone ◽  
Initial Phase ◽  
Plasma Concentrations ◽  
Compartment Model ◽  
Ovx Rats ◽  
Lh Release ◽  
Series Of Experiments ◽  
Lh Secretion ◽  
Very High

Abstract. In a first series of experiments plasma concentrations of luteinizing hormone (LH) were measured at 10 min intervals during 2 h of constant rate infusion of luteinizing hormone-releasing hormone (LRH; 104 ng/ h) in phenobarbitone-anaesthetized long-term ovariectomized (OVX) rats, treated with oil or oestradiol-benzoate (OeB). From these data the mean LH secretion rates during the sampling intervals were calculated using a one-compartment model for the elimination of LH from the plasma. It was found in the OeB-primed OVX rats that during the initial 30–40 min of infusion the LH release is high but constant. Thereafter it shows a further increase. In the oil-treated OVX rats a similar biphasic LH release pattern was found, but in these animals it was preceded by an initial phase of very high LH release, lasting a few minutes. In another series of experiments a second LRH infusion (again 104 ng/h) was given to OeB-primed OVX rats, starting 1.5 h after the discontinuation of a first LRH infusion lasting either 1, 3.5 or 20 h. The resulting secondary LH responses were smaller the longer the first infusion had lasted, but the LH secretion pattern was similar with all three time schedules and resembled the triphasic pattern observed during the first experiment in the oil-treated OVX rats, rather than the biphasic pattern of the OeB-primed OVX rats. These results indicate that the LH response to LRH of OVX rats (either treated with OeB or oil), like that of the cyclic rats, exhibits a phase of constant LH release. It is generally assumed that during this period conditions, necessary for the subsequent further increase of the LH secretion, are generated. It is concluded that these conditions largely disappear during a 1.5 h non-stimulus period. It is also concluded that the short initial phase of very high LH secretion is due to recent exposure of the LH-secretory system to stimulatory amounts of LRH.

Suppression by LRH of the stimulatory effect of oestradiol on the secretion of LH by the rat pituitary gland

1987 ◽  
Vol 114 (4) ◽  
pp. 488-496
Author(s):  
G. A. Schuiling ◽  
H. Moes ◽  
J. de Koning ◽  
T. R. Koiter
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Secretion Rate ◽  
Ovariectomized Rats ◽  
Release Mechanisms ◽  
Lh Release ◽  
Lh Secretion ◽  
Positive Effect

Abstract. Ovariectomized rats were infused with varying doses of luteinizing hormone-releasing-hormone (LRH). Some of the rats were also treated with oestradiol benzoate (EB). The effects of these pre-treatments on the in vitro release of luteinizing hormone (LH) were studied. The following parameters of in vitro LH release were measured: a) the autonomous secretion rate; b) the secretion rate following maximum stimulation with LRH, and c) the total quantity of LH released during the 6-hour experiment. The in vivo pre-treatments with LRH and EB dose-dependently decreased the pituitary LH content as well as all three of the above parameters of in vitro LH secretion. There was a linear relationship between the pituitary LH content and the three parameters of in vitro LH release. These parameters were therefore expressed as percentage of the pituitary LH content to give the relative LH secretion rates. The three parameters were thereby corrected for LRH/EB-induced changes in the pituitary LH content. In this way we obtained information on the effects of LRH and EB on the state of the LH release mechanisms of the gonadotropes. EB potentiated the LRH-induced depletion of the pituitary LH stores at all in vivo LRH infusion rates. The effect of EB on the quantity of LH released during perifusion in vitro, however, varied with the previous LRH infusion rates. After LRH infusion rates lower than about 120 ng/h (which establishes plasma concentrations of about 70 ng/l) EB enhanced the stimulated quantity of LH released. After higher rates of LRH infusion, EB lowered the amount of LH released. The effect of EB on the relative secretion of LH in vitro, i.e. on the LH release mechanisms, however, was positive irrespective of the prior in vivo LRH infusion rates, although the effect of EB was greater at the lower rates of LRH infusion. The effect of EB on the autonomous, in vitro, LH secretion rate was positive irrespective of the prior in vivo LRH infusion rates. The positive effect of EB on the mechanism underlying this component of LH secretion was LRH-independent. The effect of EB on the mechanism underlying the LRH-stimulated component of LH release appeared to be strongly LRH-dependent. The effect of EB was maximal if the LRH infusion rate had been lower than about 50 ng/h. With higher infusion rates it became increasingly smaller and was zero at the rate of about 180 ng/h or more. The LRH infusion rates of 50 and 180 ng/h establish plasma LRH concentrations of about 30 and 90 ng/l. Thus, the positive effect of EB on the LRH-stimulated component of LH secretion can be regulated by LRH at the plasma concentration interval of 30–90 ng/l. This study demonstrates that the 'overall' effect of EB on the LH secretion rate is determined by the 'balance' between the effect of EB on the pituitary LH content (the potentiation of the LRH-induced depletion of the LH stores) and the effect of EB on the LH release mechanisms (which effect, in the case of the LRH-stimulated component of LH secretion, can be suppressed by LRH). If the former effect dominates, the effect of EB on the secretion of LH is negative, if the latter dominates, the effect of EB is positive. The LRH concentration at which the positive effect turns into the negative effect is about 70 ng/l. We suggest that the ability of LRH and EB to influence each others' effect on the pituitary gland at physiological concentrations of the two hormones, plays a role in the regulation of the secretion of LH.

Adrenal progesterone facilitates the negative feedback of oestrogen on LH release in ovariectomized rats

1993 ◽  
Vol 139 (2) ◽  
pp. 253-258 ◽  
Author(s):  
A. M. Salicioni ◽  
R. W. Carón ◽  
R. P. Deis
Keyword(s):  
Ovariectomized Rats ◽  
Adrenal Steroids ◽  
Serum Progesterone ◽  
Oestrogen Treatment ◽  
Ovx Rats ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Lh Secretion

ABSTRACT There is evidence that the adrenals play a role in the regulation of the synthesis and release of gonadotrophins in various vertebrates. The aim of this study was to determine the part played by adrenal steroids, with special reference to progesterone, on the concentration of LH in ovariectomized (OVX) and oestrogen-primed rats. OVX rats received a single s.c. injection of vehicle or oestradiol benzoate (OB, 20 μg/rat). This day was designated as day 0. Three or four days later (day 3–day 4), the rats were treated with mifepristone (10 mg/kg) or with two doses of progesterone antiserum and blood samples were obtained at 13.00 and 18.00 h. OB treatment of OVX rats reduced serum LH at 13.00 h and 18.00 h on day 3 but only at 13.00 h on day 4. The administration of mifepristone at 08.00 h to OVX and oestrogen-treated rats induced a significant increase in serum LH at 18.00 h on days 3 and 4, without modifying the values at 13.00 h. When mifepristone was given at 13.00 h a much larger increase in serum LH was obtained at 18.00 h. In OVX and oestrogen-treated rats, adrenalectomy on day 2 (08.00–09.00 h) induced an increase in serum LH at 18.00 h similar to that observed in the OVX and oestrogen-primed rats after mifepristone treatment. In order to determine the specificity of the effect of mifepristone, a group of OVX and oestrogentreated rats was injected with progesterone antiserum at 08.00 and 13.00 h on day 3. Serum LH concentrations at 13.00 and 18.00 h on day 3 were similar to values obtained in OVX rats treated with oestrogen and mifepristone. Serum progesterone was measured at 08.00 and 13.00 h in OVX and OVX and oestrogenprimed rats. At both times, values were similar in OVX rats but oestrogen treatment significantly increased serum progesterone levels. The important role of adrenal progesterone on the regulation of LH secretion in OVX and oestrogen-primed rats is evident from these results. Blocking progesterone action at the receptor level, we showed that OB significantly increased LH values at 18.00 h. On the basis of these studies it is tempting to speculate on the possibility of an inhibitory or stimulatory effect of oestrogen on serum LH concentration in OVX rats, according to the presence or absence of adrenal progesterone action. Journal of Endocrinology (1993) 139, 253–258

Comparison of the LH secretion patterns in the male rat following infusion of LRH and of the LRH-analogue buserelin®. Influence of castration and oestradiol benzoate on the efficiency of LH release

1983 ◽  
Vol 102 (2) ◽  
pp. 196-204 ◽  
Author(s):  
G. A. Schuiling ◽  
N. Pols-Valkhof ◽  
T. R. Koiter
Keyword(s):  
Area Under The Curve ◽  
Male Rats ◽  
Male Rat ◽  
Potency Ratio ◽  
Maximal Height ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Buserelin Treatment ◽  
Pre Treatment ◽  
Lh Secretion

Abstract. The LH releasing activities of LRH and the LRH-analogue buserelin® (HOE 766; (D-Ser (But)6-LRH(1–9)nona peptide-ethylamide) were compared in intact and short- and long-term castrated male rats, pre-treated (either 1 or 3 days) with oestradiol benzoate (EB) or oil. LRH and buserelin were infused iv at the constant rate of 104 ng/h for 21 h. Blood samples were taken from an intracarotid cannula. LH responses were judged on the basis of the mean maximal height of the LH concentration (MH; ng LH/ml plasma) and a parameter of total LH release, i.e. the area under the curve of LH concentrations plotted against time ('area under the curve', AUC; expressed in 'area units'). The release efficiency of LRH and buserelin, E (see for a definition: Materials and Methods), which informs on the total quantity of LH released in relation to pituitary LH content, was calculated by dividing the AUC × 100 by the pituitary LH content at the beginning of stimulation. Maximal plasma LH concentrations were observed between t= 1.5 and t=3 h after LRH and between t= 1.5 and t=9 after buserelin treatment. Both with LRH and buserelin the rise of LH secretion was greater the longer the animals were castrated and/or pre-treated with EB. The buserelin-induced LH response (with the exception of the responses induced in the EB-pre-treated, 4-weeks castrated rat) were about 2–2.5 times higher (MH) and larger (AUC) than the corresponding LRH-induced responses. The buserelin/LRH potency ratio, therefore, is about 2–2.5. EB-pre-treatment did not change the pituitary LH content. It therefore enhanced the efficiency of release of LH of both LRH and buserelin. Castration, on the other hand, caused an increase of the pituitary LH content: after 4 weeks it was raised by a factor 4. Since, however, the LH responses induced by LRH and buserelin were proportionally higher and larger, castration did not significantly change the efficiency of LH release. The results indicate that the efficiency of LH release can be changed by changes in the endocrine environment in the experimental animals, whilst for the magnitude of LH responses the pituitary LH content is also important. It is therefore suggested that the responsiveness of the pituitary gland to LRH (and agonistic analogues) is determined by (1) the state of the LH secretion mechanism and (2) the pituitary LH content.

Changes in the granule population of gonadotrophs of hypogonadal (hpg) and normal female mice associated with the priming effect of LH-releasing hormone in vitro

1986 ◽  
Vol 109 (1) ◽  
pp. 35-NP ◽  
Author(s):  
C. E. Lewis ◽  
J. F. Morris ◽  
G. Fink ◽  
M. Johnson
Keyword(s):  
Priming Effect ◽  
Marginal Zone ◽  
Secretory Granules ◽  
Initial Exposure ◽  
Releasing Hormone ◽  
Female Mice ◽  
Mean Diameter ◽  
Lh Release ◽  
The Mean ◽  
Lh Releasing Hormone

ABSTRACT Changes in the size and position of secretory granules in pituitary gonadotrophs have been studied in relationship to LH release and self-priming induced by LH-releasing hormone (LHRH) in pituitary glands from normal and hypogonadal (hpg) female mice. Hemipituitary glands were preincubated and then incubated for either 1 or 2 h in the absence or presence of LHRH (8·5 nmol/l). The glands were either processed for ultrastructural morphometry or homogenized for the determination of pituitary LH content. Morphometry was carried out on gonadotrophs identified by immunocytochemistry for LHβ using the thin/semi-thin section method. Pituitary LH content and the amount of LH released were determined by radioimmunoassay. The amount of LH released in response to the first and second hours of incubation with LHRH were similar in hpg and normal mice with a clear priming effect (three- to fourfold increase in pituitary responsiveness to LHRH) occurring in both strains. Despite a substantially reduced total number of granules (and amount of LH) in unstimulated hpg gonadotrophs, the number of granules in the outer 500 nm marginal zone of the cells was similar to that in normal mice. This could explain the similar amount of LH released from normal and hpg glands by the first LHRH challenge. The initial exposure to LHRH was also associated with a marked translocation of secretory granules from the central to the outer marginal region of cytoplasm subjacent to the gonadotroph plasmalemma, such that in 'primed' glands 60% of granules were found in this marginal zone compared with 40% (hpg) or 33% (normal) in unstimulated glands. The mean diameter of granules in the marginal zone was significantly less than that of granules in the central zone of the gonadotrophs of unstimulated glands from both normal and hpg animals. Exposure to LHRH for 1 h was associated with an increase in the number of small granules in the marginal zone and a significant decrease in the mean diameter of the gonadotroph granule population as a whole. After the primed release of LH, increased proportions of granules were still located in the marginal zone of gonadotrophs, indicating that granule migration continued during the second hour of exposure to LHRH in which primed release occurred. The primed release was associated with a detectable reduction in both the LH and granule content of gonadotrophs in normal, but not hpg glands. The ultrastructural correlates of LH release and LHRH priming were similar in the two strains of mice, and therefore in mice neither the releasing nor the priming effect of LHRH depends upon previous exposure of the pituitary gland to LHRH or ovarian factors. The priming effect was associated with a marked shift of granules towards the plasmalemma and a decrease in granule size which most likely resulted from increased post-translational processing within secretory granules. J. Endocr. (1986) 109, 35–44

EFFECT OF AN ANABOLIC STEROID (METANDIENON) ON PLASMA LH, FSH, AND TESTOSTERONE AND ON THE RESPONSE TO INTRAVENOUS ADMINISTRATION OF LRH

1976 ◽  
Vol 83 (4) ◽  
pp. 856-864 ◽  
Author(s):  
Pentti Holma ◽  
Herman Adlercreutz
Keyword(s):  
Luteinizing Hormone ◽  
Intravenous Administration ◽  
Anabolic Steroid ◽  
Plasma Levels ◽  
Oral Intake ◽  
Plasma Testosterone ◽  
Before And After ◽  
The Mean ◽  
Pre Treatment ◽  
Lh Secretion

ABSTRACT Plasma levels of testosterone, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) as well as the response of LH and FSH to the intravenous administration of 100 μg of luteinizing hormone releasing hormone (LRH) were measured in 16 well-trained athletes (mean age 30 years) before and after 2 months of daily oral intake of 15 mg of metandienon, an anabolic steroid (Anabolin®, 17α-methyl-17β-hydroxy-1,4-androstadien-3-one, Medica, Finland). All athletes continued to train regularly, just as they had done for several years. During administration of metandienon the mean plasma testosterone level fell 69%, from 29.4 ± 11.6 nmol/l to 9.1 ± 7.5 nmol/l. The mean plasma levels of LH and FSH also fell significantly (P < 0.001 and P < 0.01, respectively), both about 50%. Because LH and FSH levels were low after administration of the steroid the maximum stimulation values after LRH administration were also lower than pre-treatment values although the mean increments did not differ significantly before and after administration of the anabolic steroid. However, after treatment, the FSH response curve had a biphasic pattern in most subjects, with peaks at 10 to 20 and 50 to 60 min after the iv injection of LRH. Administration of LRH after the treatment period had no effect on FSH secretion in two subjects and no effect on LH secretion in one. Our results show that administration of an anabolic steroid causes a pronounced lowering of plasma levels of testosterone, LH and FSH but causes no gross alteration in the response of LH secretion to stimulation by LRH. The reason for the biphasic response pattern of FSH to LRH administration in most subjects is not known.

The effect of gonadotrophin surge-inhibiting factor on the self-priming action of gonadotrophin-releasing hormone in female rats in vitro

1992 ◽  
Vol 134 (3) ◽  
pp. 427-436 ◽  
Author(s):  
D. W. Koppenaal ◽  
A. M. I. Tijssen ◽  
J. de Koning
Keyword(s):  
Protein Synthesis ◽  
Priming Effect ◽  
The Self ◽  
Pituitary Cells ◽  
Inhibiting Factor ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Functional Antagonism

ABSTRACT The present study was designed to explore further the functional antagonism between gonadotrophin-releasing hormone (GnRH) and the ovarian factor, gonadotrophin surge-inhibiting factor (GnSIF). In all experiments, pituitary tissue was exposed to various amounts of GnSIF, after which the self-priming action of GnRH was studied. GnSIF was increased in vivo by FSH treatment and increased in vitro by adding various amounts of follicular fluid (FF) to cultured pituitary cells. Treatment with 3 or 10 IU FSH suppressed the initial LH response and delayed the maximally primed LH response to GnRH. Treatment with FSH was only effective in intact rats on days 1 and 2 of dioestrus. There was no difference in the rate of maximal LH release irrespective of treatment with either FSH or saline. Since FSH treatment was ineffective in long-term ovariectomized rats, it was concluded that the initial suppressive effect of FSH on LH release was mediated by GnSIF. Cycloheximide prevented the self-priming action of GnRH by inhibiting GnRH-induced protein synthesis. The initial protein synthesis-independent GnRH-stimulated LH release, which was already suppressed by FSH treatment, remained suppressed in the presence of cycloheximide. Pretreatment with GnRH in vivo increased the protein synthesis-independent GnRH-induced LH release during subsequent incubation of the glands. This increase did not occur after FSH treatment. Pituitary cells, cultured for 20 h in medium only, failed to elicit the self-priming effect of GnRH. Preincubation with FF maintained the self-priming effect. This was independent of the concomitant presence of various amounts of oestradiol. Preincubation with bovine FF suppressed the initial GnRH-stimulated LH release dose-dependently. Porcine FF, human FF and testicular extract suppressed the release of LH in a similar way. It was concluded that GnSIF suppresses the initial LH response to continuous GnRH stimulation. Increased levels of GnSIF caused by FSH treatment also delayed the primed LH release. The mechanism of functional antagonism between GnSIF and GnRH could give rise to the occurrence of the phenomenon of GnRH self-priming. Journal of Endocrinology (1992) 134, 427–436

Na+ secretion rate increases proportionally more than the Na+ reabsorption rate with increases in sweat rate

2008 ◽  
Vol 105 (4) ◽  
pp. 1044-1048 ◽  
Author(s):  
Michael J. Buono ◽  
Ryan Claros ◽  
Teshina DeBoer ◽  
Janine Wong
Keyword(s):  
Sweat Rate ◽  
Physiological Mechanism ◽  
Exercise Bout ◽  
Eccrine Sweat Gland ◽  
Linear Increase ◽  
Secretion Rate ◽  
Blood Samples ◽  
The Mean ◽  
Reabsorption Rate

The purpose of this study was to measure the in vivo Na+ secretion and Na+ reabsorption rates of the human eccrine sweat gland with increases in sweat rate. Such data should help to elucidate the physiological mechanism responsible for the previously reported linear relationship between increases in sweat rate and Na+ concentration in sweat. On 5 days, each subject ( n = 10) completed a 30-min exercise bout in an environmental chamber set at 35°C and 40% relative humidity. The intensity for the five exercise bouts in the heat was set to approximate 50, 60, 70, 80, and 90% of age-predicted maximum heart rate. Forearm sweat samples and capillary blood samples were collected during each of the five 30-min exercise bouts. The sweat and blood samples were analyzed for Na+ concentration in sweat and serum, which were used to calculate the rate of Na+ secretion and Na+ reabsorption. The mean correlation between sweat rate and Na+ concentration in sweat was found to be r = 0.73. Within the sweat rate range of the present study, both Na+ secretion rate and Na+ reabsorption rate increased linearly; however, the Na+ secretion rate increased almost twice as fast (slope = 141 vs. 80). Thus the rate at which Na+ escaped reabsorption increased with increases in sweat rate and was significantly ( P < 0.05) correlated to the Na+ concentration in sweat (mean r = 0.90). Such results strongly suggest that the physiological mechanism responsible for the previously reported linear increase in Na+ concentration in sweat seen with increases in sweat rate is that the Na+ secretion rate increases proportionally more than the Na+ reabsorption rate.

scholarly journals Unsaturated Fatty Acids Stimulate LH Secretion via Novel PKCε and -θ in Gonadotrope Cells and Inhibit GnRH-Induced LH Release

Endocrinology ◽  
2011 ◽  
Vol 152 (10) ◽  
pp. 3905-3916 ◽  
Author(s):  
Ghislaine Garrel ◽  
Violaine Simon ◽  
Chantal Denoyelle ◽  
Céline Cruciani-Guglielmacci ◽  
Stéphanie Migrenne ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Cell Cultures ◽  
Unsaturated Fatty Acids ◽  
Reproductive Function ◽  
Peroxisome Proliferator ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Lh Release ◽  
Lh Secretion

The activity of pituitary gonadotrope cells, crucial for reproductive function, is regulated by numerous factors including signals related to nutritional status. In this work, we demonstrated, for the first time, that in vivo central exposure of rats to lipids intracarotid infusion of a heparinized triglyceride emulsion selectively increases the expression of pituitary LH subunit genes without any alteration of pituitary GnRH receptor and hypothalamic GnRH or Kiss-1 transcript levels. Furthermore, we showed that unsaturated fatty acids (UFA), oleate and linoleate, increase LH release in a dose-dependent manner as well as LHβ mRNA levels in both immortalized LβT2 gonadotrope cell line and rat primary cell cultures. In contrast, the saturated palmitate was ineffective. ACTH or TSH secretion was unaffected by UFA treatment. We demonstrated in LβT2 cells that linoleate effect is mediated neither by activation of membrane fatty acid (FA) receptors GPR40 or GPR120 although we characterized these receptors in LβT2 cells, nor through nuclear peroxisome proliferator-activated receptors. Furthermore, linoleate β-oxidation is not required for its action on LH secretion. In contrast, pharmacological inhibition of protein kinase C (PKC) or ERK pathways significantly prevented linoleate-stimulated LH release. Accordingly, linoleate was shown to activate novel PKC isoforms, PKCε and -θ, as well as ERK1/2 in LβT2 cells. Lastly, unsaturated, but not saturated, FA inhibited GnRH-induced LH secretion in LβT2 cells as well as in pituitary cell cultures. Altogether, these results suggest that the pituitary is a relevant site of FA action and that UFA may influence reproduction by directly interfering with basal and GnRH-dependent gonadotrope activity.

Sign in / Sign up

Export Citation Format

Share Document