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Spermatogenesis is an extraordinarily complex process, regulated by several factors, which leads to the differentiation of spermatogonia into spermatozoa. Among vertebrates, several reports have been focused on the lizard Podarcis sicula, a seasonal breeder and a good model for the study of reproductive processes. The goal of this review is to resume all the available data about systemic and above all local control factors involved in the control of P. sicula testicular activity. During the seasonal reproductive cycle, the variation of the expression levels of these factors determines significant variations that induce the activation or blocking of spermatogenesis. The data supplied in this review, in addition to analyze the current literature regarding the main actors of Podarcis sicula spermatogenesis, will hopefully provide a basic model that can be used for further studies on the intratesticular interaction between molecular factors that control spermatogenesis.

The classical concepts of human sodium balance include 1) a total pool of Na+ of ≈4,200 mmol (total body sodium, TBS) distributed primarily in the extracellular fluid (ECV) and bone, 2) intake variations of 0.03 to ≈6 mmol·kg body mass−1·day−1, 3) asymptotic transitions between steady states with a halftime (T½) of 21 h, 4) changes in TBS driven by sodium intake measuring ≈1.3 day [ΔTBS/Δ(Na+ intake/day)], 5) adjustment of Na+ excretion to match any diet thus providing metabolic steady state, and 6) regulation of TBS via controlled excretion (90–95% renal) mediated by surrogate variables. The present focus areas include 1) uneven, nonosmotic distribution of increments in TBS primarily in “skin,” 2) long-term instability of TBS during constant Na+ intake, and 3) physiological regulation of renal Na+ excretion primarily by neurohumoral mechanisms dependent on ECV rather than arterial pressure. Under physiological conditions 1) the nonosmotic distribution of Na+ seems conceptually important, but quantitatively ill defined; 2) long-term variations in TBS represent significant deviations from steady state, but the importance is undetermined; and 3) the neurohumoral mechanisms of sodium homeostasis competing with pressure natriuresis are essential for systematic analysis of short-term and long-term regulation of TBS. Sodium homeostasis and blood pressure regulation are intimately related. Real progress is slow and will accelerate only through recognition of the present level of ignorance. Nonosmotic distribution of sodium, pressure natriuresis, and volume-mediated regulation of renal sodium excretion are essential intertwined concepts in need of clear definitions, conscious models, and future attention.

In this study, we examined the effects of porcine growth hormone (GH) and cortisol on plasma insulin-like growth factor binding proteins (IGFBPs) in juveniles of three subspecies of Oncorhynchus masou (masu, amago, and Biwa salmon). Ligand blotting using digoxigenin-labeled human IGF-I was used to detect and semi-quantify three major circulating IGFBP bands at 41, 28, and 22 kDa, corresponding to IGFBP-2b, −1a, and -1b, respectively. GH increased plasma IGFBP-2b concentration in masu and Biwa salmon but suppressed it in amago salmon. Plasma IGFBP-2b levels were increased by cortisol in the three subspecies. Cortisol induced plasma IGFBP-1a in the three subspecies, whereas GH had a suppressive effect in masu and Biwa salmon. Sham and cortisol injections increased plasma IGFBP-1b levels after 1 day in masu and amago salmon, suggesting that IGFBP-1b is induced following exposure to stressors via cortisol. Increased IGFBP-1b levels were restored to basal levels when co-injected with GH in Biwa salmon, and the same trend was seen in masu and amago salmon. However, the suppressive effect of GH disappeared 2 days after injection in the three subspecies. Despite some differences among subspecies, the findings suggest that cortisol is a primary inducer of plasma IGFBP-1b; however, GH counteracts it in the short term. Therefore, GH has the potential to modulate the degree of increase in circulating IGFBP-1b levels during acute stress.

Much of our understanding of the molecular control of menstruation arises from laboratory models that experimentally recapitulate some, but not all, aspects of uterine bleeding observed in women. These models include: in vitro culture of endometrial explants or isolated endometrial cells, transplantation of human endometrial tissue into immunodeficient mice and the induction of endometrial breakdown in appropriately pretreated mice. Each of these models has contributed to our understanding of molecular and cellular mechanisms of menstruation, but nonhuman primates, especially macaques, are the animal model of choice for evaluating therapies for menstrual disorders. In this chapter we review some basic aspects of menstruation, with special emphasis on the macaque model and its relevance to the clinical issues of irregular and heavy menstrual bleeding (HMB).

Introduction Of the nearly 1.4 million new cases of breast cancer diagnosed each year, a large proportion is characterized as hormone receptor negative, lacking estrogen receptors (ER) and/or progesterone receptors (PR). Patients with receptor-negative tumors do not respond to current steroid hormone-based therapies and generally have significantly higher risk of recurrence and mortality compared with patients with tumors that are ER- and/or PR-positive. Previous in vitro studies had shown that the progesterone metabolites, 5α-dihydroprogesterone (5αP) and 3α-dihydroprogesterone (3αHP), respectively, exhibit procancer and anticancer effects on receptor-negative human breast cell lines. Here in vivo studies were conducted to investigate the ability of 5αP and 3αHP to control initiation, growth, and regression of ER/PR-negative human breast cell tumors. Methods ER/PR-negative human breast cells (MDA-MB-231) were implanted into mammary fat pads of immunosuppressed mice, and the effects of 5αP and 3αHP treatments on tumor initiation, growth, suppression/regression, and histopathology were assessed in five separate experiments. Specific radioimmunoassays and gas chromatography-mass spectrometry were used to measure 5αP, 3αHP, and progesterone in mouse serum and tumors. Results Onset and growth of ER/PR-negative human breast cell tumors were significantly stimulated by 5αP and inhibited by 3αHP. When both hormones were applied simultaneously, the stimulatory effects of 5αP were abrogated by the inhibitory effects of 3αHP and vice versa. Treatment with 3αHP subsequent to 5αP-induced tumor initiation resulted in suppression of further tumorigenesis and regression of existing tumors. The levels of 5αP in tumors, regardless of treatment, were about 10-fold higher than the levels of 3αHP, and the 5αP:3αHP ratios were about fivefold higher than in serum, indicating significant changes in endogenous synthesis of these hormones in tumorous breast tissues. Conclusions The studies showed that estrogen/progesterone-insensitive breast tumors are sensitive to, and controlled by, the progesterone metabolites 5αP and 3αHP. Tumorigenesis of ER/PR-negative breast cells is significantly enhanced by 5αP and suppressed by 3αHP, the outcome depending on the relative concentrations of these two hormones in the microenvironment in the breast regions. The findings show that the production of 5αP greatly exceeds that of 3αHP in ER/PR-negative tumors and that treatment with 3αHP can effectively block tumorigenesis and cause existing tumors to regress. The results provide the first hormonal theory to explain tumorigenesis of ER/PR-negative breast tissues and support the hypothesis that a high 3αHP-to-5αP concentration ratio in the microenvironment may foster normalcy in noncancerous breast regions. The findings suggest new diagnostics based on the relative levels of these hormones and new approaches to prevention and treatment of breast cancers based on regulating the levels and action mechanisms of anti- and pro-cancer progesterone metabolites.

Numerous factors in the hypothalamus-pituitary-gonadal axis (HPG) are involved in the timing of puberty onset.Leptin signals the nutritional status and the presence of an adequate amount of loaded adipose tissue, as a long-term resource of energy, to the brain which in response switches on the reproduction process (i.e. puberty onset).The growth hormone-insulin-like growth factor I (GH/IGF-I) axis is also thought to be involved in the timing of puberty onset.The aim of this thesis was to test the hypothesis that leptin may directly or indirectly via theGH/IGFI-I axistrigger the onset of puberty onset in female rats.First, we carried out a series of descriptive and basic studies.Time of puberty onset was monitored by scoring the moment of vaginal opening (VO).The data showed a strong positive correlation between body fat and leptin levels, and showed leptin is increasing over the prepubertal period. Then, we aimed to find out the effects of food-restriction (FR) on puberty onset, body fat, plasma leptin levels and body temperature. FR postponed time of VO.Body fat, plasma leptin levels and body temperature in the FR rats were significantly lower than the controls throughout the experiment.To find outif leptin is the signal initiating the onset of puberty, we used FR rats as a model for delayed puberty onset, and centrally (icv) or peripherally (sc) administered leptin, or we centrally (icv) immunoneutralized leptin. Central leptin infusion not only restored the delay in puberty onset caused by food restriction but also advanced sexual maturation in normally fed animals.Like central infusion, also peripheral leptin infusion restored puberty onset in FR animals. So, we showed an advancing effect of both centrally and peripherally infused leptin on puberty onset in prepubertal female rats.The central immunoneutralization of leptin on the other hand, postponed puberty onset. We therefore conclude that leptin is one of the crucial factors triggering puberty onset in female rats.In the FR model system we then centrally (icv) infused GH.The infusion of GH postponed puberty onset in normally fed rats, but advanced puberty onset in FR animals. Also,the plasma leptin levels in the GH-infused animals were significantly higher than their controls and increased as GH infusion proceeded.Central infusion of GH antiserum (AS) advanced puberty onset in the pair-fed animals but not in the ad lib-fed animals. Also the central infusion of somatostatin worked likewise in both groups. These findings match with the results of the central infusion of GH which also advanced puberty onset in FR animals only.Finally, we centrally (icv) infused IGF-I in FR rats. Central infusion of IGF-I significantly postponed puberty onset in ad libitum fed animals.Immunoneutralization of endogenous IGF-I enhanced prevailing plasma leptin levels, but there was no effect on the timing of puberty onset. Centrally-present endogenous IGF-I does not appear to be involved in puberty onset although it seems to inhibit leptin secretion.In conclusion, our findings provide further evidence that leptin, a hormone produced mainly by adipose tissue, is an important and crucial signal between the bodily nutritional status and the brain (i.e. the hypothalamus) to trigger puberty onset. Furthermore, we suggest that there is a functional interaction between growth hormone (GH) and leptin to initiate puberty in female rats.

Numerous factors in the hypothalamus-pituitary-gonadal axis (HPG) are involved in the timing of puberty onset.Leptin signals the nutritional status and the presence of an adequate amount of loaded adipose tissue, as a long-term resource of energy, to the brain which in response switches on the reproduction process (i.e. puberty onset).The growth hormone-insulin-like growth factor I (GH/IGF-I) axis is also thought to be involved in the timing of puberty onset.The aim of this thesis was to test the hypothesis that leptin may directly or indirectly via theGH/IGFI-I axistrigger the onset of puberty onset in female rats.First, we carried out a series of descriptive and basic studies.Time of puberty onset was monitored by scoring the moment of vaginal opening (VO).The data showed a strong positive correlation between body fat and leptin levels, and showed leptin is increasing over the prepubertal period. Then, we aimed to find out the effects of food-restriction (FR) on puberty onset, body fat, plasma leptin levels and body temperature. FR postponed time of VO.Body fat, plasma leptin levels and body temperature in the FR rats were significantly lower than the controls throughout the experiment.To find outif leptin is the signal initiating the onset of puberty, we used FR rats as a model for delayed puberty onset, and centrally (icv) or peripherally (sc) administered leptin, or we centrally (icv) immunoneutralized leptin. Central leptin infusion not only restored the delay in puberty onset caused by food restriction but also advanced sexual maturation in normally fed animals.Like central infusion, also peripheral leptin infusion restored puberty onset in FR animals. So, we showed an advancing effect of both centrally and peripherally infused leptin on puberty onset in prepubertal female rats.The central immunoneutralization of leptin on the other hand, postponed puberty onset. We therefore conclude that leptin is one of the crucial factors triggering puberty onset in female rats.In the FR model system we then centrally (icv) infused GH.The infusion of GH postponed puberty onset in normally fed rats, but advanced puberty onset in FR animals. Also,the plasma leptin levels in the GH-infused animals were significantly higher than their controls and increased as GH infusion proceeded.Central infusion of GH antiserum (AS) advanced puberty onset in the pair-fed animals but not in the ad lib-fed animals. Also the central infusion of somatostatin worked likewise in both groups. These findings match with the results of the central infusion of GH which also advanced puberty onset in FR animals only.Finally, we centrally (icv) infused IGF-I in FR rats. Central infusion of IGF-I significantly postponed puberty onset in ad libitum fed animals.Immunoneutralization of endogenous IGF-I enhanced prevailing plasma leptin levels, but there was no effect on the timing of puberty onset. Centrally-present endogenous IGF-I does not appear to be involved in puberty onset although it seems to inhibit leptin secretion.In conclusion, our findings provide further evidence that leptin, a hormone produced mainly by adipose tissue, is an important and crucial signal between the bodily nutritional status and the brain (i.e. the hypothalamus) to trigger puberty onset. Furthermore, we suggest that there is a functional interaction between growth hormone (GH) and leptin to initiate puberty in female rats.

Fifteen tagged female sea bass Dicentrarchus labrax were sampled weekly from September to April and plasma vitellogenin (VTG), testosterone (T), 17β-estradiol (E2), and two potential maturation inducing steroids (MISs): 17,20β-dihydroxy-4-pregnen-3-one (17,20βP) and 17,20β,21-trihydroxy-4-pregnen-3-one (20βS) assayed. An oocyte sample was obtained via intraovarian cannulation at each sampling time from every female and the stage of development of the most advanced clutch of oocytes determined and related to VTG and hormone plasma levels for each female. The mean number of ovulations per female was 1·75 ± 0·25 when those females that did not present ovulations were excluded and up to 4 ovulations detected in some females. The highest plasma levels of T (c. 6 ng ml-1) were observed during postvitellogenesis and the beginning of maturation while maximum plasma levels of E2 (>5 ng ml-1) were obtained during late vitellogenesis. VTG plasma levels increased throughout vitellogenesis peaking (c. 2·5 mg ml-1) at postvittelogenesis. For the first time significant changes of plasma progestogens were detected in European sea bass during the sexual cycle. The highest plasma level of 17,20βP (c. 1·1 ng ml-1) was observed during postvitellogenesis while the highest level of 20βS (c. 1·4 ng ml-1) coincided with final maturation. These results suggest that 17,20βP and 20βS play a role in the early and final maturation, respectively, in the European sea bass., This studywas supported by EEC (AIR-CT93-1005) and CICYT (MAR96-1859) and by theSpanish Ministry of Education and Culture and British Council through an IntegratedAction grant (HB1997-0072) to M.C. and D.E.K. J.F.A. was supported by the Generalitat Valenciana

In the present study, we have characterized the beta 2-adrenergic receptor (beta 2-AR)-adenosine 3',5'-cyclic monophosphate (cAMP) system of the rat thymus gland and examined the hormonal regulation of the thymic beta 2-AR gene expression under physiological or pharmacological conditions accompanied by marked alterations of the sex steroid hormone milieu. We report here that membrane preparations of female rat thymic tissue contain iodocyanopindolol binding sites that exhibit pharmacological properties typical of a beta-AR. Detailed analysis by computer modeling of the binding potencies of a large series of beta 1- and beta 2-adrenergic agonists and antagonists revealed predominantly the beta 2-AR subtype (78%) in rat thymus. This inference from radioligand binding studies was corroborated functionally by the rank order of potencies of a series of adrenergic agonists to stimulate the production of cAMP. Northern blot analysis, using a human beta 2-AR cDNA as a probe, revealed the presence of a mRNA of 2.3 kb, which is consistent with the size of the beta 2-AR mRNA found in other rat tissues. Physiological regulation of specific beta 2-AR in the rat thymus was indicated by significant increases in both receptor concentration and steady-state levels of beta 2-AR mRNA during the diestrous 2 and proestrous phases of the rat estrous cycle and pregnancy, whereas castration sharply reduced beta 2-AR numbers and transcript levels within the thymus. The modulation of the thymic beta 2-AR-cAMP signaling system by the preexisting sex steroid milieu, coupled with the sex-dependent adrenergic modulation of thymic cell-mediated immune response, may contribute to the various sex-related alterations in immune responsiveness and could play a role in sexually related immune disorders.

The eggs from oviparous organisms contain large amounts of vitellus, or yolk, which are utilized by the growing embryo. Vitellogenesis is the process of vitellus accumulation and involves massive heterosynthetic synthesis of the protein vitellogenin (Vg) and its deposition in the oocyte. This work summarizes data on Vg structure, synthesis, uptake by oocytes and its fate during embryogenesis. The hormonal control of vitellogenesis and its tissue, sex and temporal regulation are also discussed. Where it is available, data on structure and expression of Vg-coding genes are reviewed. Insect vitellogenesis is priorized although other oviparous animal groups outside insects are also treated.

The effect of melatonin on wool quality and thyroid function was studied. Ten ewes received a melatonin implant (M) on March 2004, and 10 ewes which were not implanted served as control (C). At monthly intervals over 12 months, fibre length and growth were calculated, and plasma thyroxine (T4) concentrations were measured. Wool samples (~N = 2000 fibres) were collected and fibre diameter, standard deviation and coefficient of variation of fibre diameter, spin fineness, comfort factor, 5% of fibres «x» µm above the mean diameter, curve, and clean yield were measured. In summer, M ewes had significantly lower plasma T4 concentrations than C ewes, with significant group (P < 0.05) and season (P < 0.01) effects. Melatonin ewes produced shorter wool than C ewes (P < 0.001) and, in autumn, the differences were statistically significant. Fibre growth did not differ significantly between groups. Throughout the year, M ewes produced wool with a fibre diameter (mean = 26.5 ± 0.2 µm) that was significantly (P < 0.01) shorter than C wool (means = 27.2 ± 0.5 µm). Overall, the melatonin treatment had a significant (P < 0.01) effect on mean comfort factor, and the differences between groups were significant (P < 0.05) in summer and autumn. The overall annual mean curve value of wool produced by M ewes (80.9 ± 1.7) was significantly (P < 0.01) lower than wool produced by C ewes (82.8 ± 1.3) and, in winter, the difference between groups was significant (P < 0.05). In conclusion, exogenous melatonin in spring positively affected medium- and long-term measures of wool quality. The physiological processes mediating these mechanisms remain to be elucidated.

The effect of a juvenile hormone analogue, S-71639, was tested on the eggs, four larval instars and adults of the Colorado potato beetle, Leptinotarsa decemlineata Say, by topical application or after treatment of the foodplant. The last larval instar is very sensitive to S-71639. Treatment of this instar delayed the onset of pupation and prevented adult emergence. Treated animals showed severe abnormalities, but they were not immediately killed at the doses used in this study. Treatment of larvae also interfered with the photoperiodic induction of diapause. Adults, kept under diapausing conditions, started to lay eggs after treatment with S-71639. The ovicidal effect of the compound was rather weak. The implications for practical use of S-71639 in control of the Colorado potato beetle are being discussed. Resume Effets d'un analogue d'hormone juvenile sur les oeufs, le developpement post-embryonic, la metamorphose et l'induction de la diapause chez le doryphore, Leptinotarsa decemlineata L'effet d'un analogue de l'hormone juvenile, S-71639, a ete teste sur les oeufs, les quatre stades larvaires et les adultes du doryphore, Leptinotarsa decemlineata Say, par application topique ou apres traitement de la plante-hote. Le dernier stade larvaire est tres sensible au S-71639. Le traitement de ce stade retarde le debut de la metamorphose et empeche l'emergence adulte. Les animaux traites montrent de graves anomalies, mais ne sont pas immediatement tues par les doses utilisees dans cette etude. Le traitement des larves perturbe aussi l'induction photoperiodique de la diapause. Les adultes places dans des conditions de diapause, commencent a pondre apres traitement au S-71639. L'effet ovicide de la substance est plutot faible. Les implications pour l'utilisation pratique du S-71639 dans la lutte contre le doryphore sont discutees.

The modulation of brain LHRH receptors by sex steroids was assessed in the female rat hippocampus using in vitro autoradiography and iodinated [D-Ser (TBU) 6 , des-Gly-NH 2 10 ]LHRH ethylamide as the radioligand. As evaluated by optical densitometry, the density of hippocampal LHRH receptors was increased by castration. In castrated animals, estradiol administration produced a small decrease in receptor concentration, whereas the concomitant administration of progesterone and estradiol as well as the injection of dihydrotestosterone induced a marked decrease in receptor density. Progesterone administration did not produce any significant change in receptor concentration. These results indicate that brain LHRH receptors can be modulated by sex steroids. Interestingly, this modulation of hippocampal LHRH receptors is similar to that previously observed in pituitary gland.