Low LH Levels Research Articles

Androgen and estrogen response to adrenal and gonadal stimulation in idiopathic hemochromatosis: evidence for decreased estrogen formation.

Gonadal function in idiopathic hemochromatosis (IHC) was evaluated by comparing clinical features and levels of sex hormones in 10 male patients with IHC (cirrhosis, 4; fibrosis, 6), 6 male patients with alcoholic cirrhosis (AC) and 10 healthy, age-matched controls. Impotence was present in 9 IHC and all AC patients and was associated with decreased plasma testosterone levels. However, gynecomastia, a feature in all patients with AC, was not present in IHC, and plasma sex hormone binding globulin was normal. Patients with IHC showed significantly lower basal estradiol levels (17.7 +/- 6.3 pg per ml) than did controls (28.5 +/- 8.5 pg per ml), and low LH levels (p less than 0.01), which were insufficiently stimulated by luteinizing hormone releasing hormone (n = 8) as well as a decrease in prolactin concentration (2.9 +/- 1.4 vs. 5.9 +/- 1.9 ng per ml in the controls) suggesting pituitary failure. Synthesizing capacity of sex hormones was determined by adrenocorticotropic hormone and human chorionic gonadotropin administration. Basal and stimulated levels of androstenedione and cortisol indicated normal function of the adrenals in IHC. However after adrenocorticotropic hormone, estrone levels increased to only 16.2 +/- 8.4 pg per ml (controls, 27.3 +/- 4.7 pg per ml; p less than 0.01). Increments of estrone (12.5 +/- 9.2 pg per ml) and estradiol (17.9 +/- 11.6 pg per ml) were also lower in IHC following human chorionic gonadotropin administration than in controls (26.0 +/- 7.2 and 37.5 +/- 11.4 pg per ml, respectively). In contrast, plasma human chorionic gonadotropin raised testosterone levels 3.3-fold in IHC and 2.2-fold in controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Low serum levels of FSH, LH and prolactin in luteal phase inadequacy.

In order to elucidate the relationship between prolactin (PRL) levels and corpus luteum function in humans, assessment of temporal relationship between levels of PRL, LH, FSH, estradiol and progesterone was made in eleven normal cycling women and six short luteal women. All hormones were determined by specific radioimmunoassay. The mean PRL level in the luteal phase was higher than that in the follicular phase in normal women. On the other hand, no difference mean was seen between the PRL levels of follicular and luteal phases in short luteal women. In addition, follicular and luteal phase secretion of PRL in the short luteal phase (SLP) was lower than that in the normal control. LH and FSH in the follicular and luteal phases, estradiol secretion in the late follicular and early to mid-luteal phases in SLP were also lower than those in the control. These observations were consistent with the hypothesis that SLP is a sequel to aberrant folliculogenesis. In addition, it is inferred that low PRL levels in the SLP might be due to inadequate augmentation by estrogen, rather than giving PRL any positive controlling role in the maintenance of corpus luteum function.

The inhibitory effect of opiates on gonadotrophin secretion is dependent upon gonadal steroids.

We have attempted to clarify the physiological involvement of endogenous opiates in the steroid-mediated control of gonadotrophin release. Our studies showed that there was an acute reduction in the inhibitory effects of endogenous opiates on LH and FSH release following gonadectomy in the rat. This was indicated by a significant reduction in the ability of naloxone to stimulate serum LH/FSH levels (sampled at 15 min) in 26-day-old female rats 48 h after ovariectomy. Luteinizing hormone was highly sensitive to the inhibitory effects of the synthetic met-enkephalin analogue, FK 33-824, at this time (sampled at 90 min). An unexpected observation was that long-term absence of gonadal steroids also disrupted the ability of exogenous opiates, FK 33-824 and morphine, to influence LH release. This was seen as an inability of FK 33-824 (1.0 or 3.0 mg/kg) to inhibit LH secretion. The effects of gonadectomy on opiate control of LH occurred at all developmental stages and were not due to a disruption of sexual maturation. Opiate involvement in prolactin secretion did not appear to be adversely affected by an absence of gonadal steroids. Another novel aspect of this work was that the opiatergic component in the control of gonadotrophin secretion could be reinstated in long-term gonadectomized rats by treatment with oestradiol benzoate or testosterone propionate. Similarly, priming with increasing dosages of oestradiol benzoate which resulted in progressively lower LH levels gave larger naloxone in progressively lower LH levels gave larger naloxone responses.(ABSTRACT TRUNCATED AT 250 WORDS)

McCUNE ALBRIGHT SYNDROME - EVIDENCE OF AUTONOMOUS ENDOCRINE FUNCTION

The origin of sexual precocity in McCune Albright Syndrome is still in question, whether hypothalmic or ovarian in origin. We studied a 5 year old girl who presented with breast enlargement, episodes of menstrual bleeding, pubic and axillary hair and right sided facial prominence. She had radiological evidence of polyostotic fibrous dysplasia and ultrasound evidence of ovarian cysts. A Neuroendocrine workup was done which demonstrated low basal levels of LH and FSH and failure to respond to GnRH, but her Serum Estradiol levels on two occasions were elevated (52 pg/ml and 18 pg/ml).Thyroid functions were normal and TRH Stimulation Test showed a normal TSH and Prolactin response. Somatomedin-C by RIA was 2.7 U/ml (Normal 0.8-2.4). Serum Cortisol was normal. Wedge resection of the ovaries was done after which her Estradiol fell to 9 pg/ml and there has been regression in her breast size, no further menstrual bleeding and no evidence of progression of sexual precocity during short term follow up. Our studies and follow up indicate that the sexual precocity in McCune Albright Syndrome is ovarian in origin. Long term follow up is continuing.

Periodic exposure to a brief light signal stimulates neuroendocrine-gonadal activity in golden hamsters.

The photoperiodic effects of a periodic light pulse on neuroendocrine-gonadal activity in the male golden hamster was examined using a night interruption paradigm. Adult male hamsters that had been housed 3 to 5 per cage on LD 14:10 were placed either in individual cages, each equipped with a running wheel, or maintained in communal housing conditions, without access to a running wheel. Animals were then transferred to either LD 6:18 or to a LD 6:18 light cycle with a periodic 10-second night interruption (8 hours after lights off) occurring once every two, four, or seven days. As expected, exposure to LD 6:18 for 11 weeks induced complete regression of the testes and seminal vesicles, accompanied by low serum levels of LH and FSH, in both individually and communally-housed animals. However, in individually-housed animals receiving a 10-second night interruption every other day on LD 6:18, paired testis and seminal vesicle weights, as well as serum gonadotropin levels, were maintained at values comparable to those normally observed in hamsters exposed to photostimulatory long days. Furthermore, the presentation of a periodic 10-second night interruption once every four or seven days to individually-housed animals with access to a running wheel was sufficient to partially or totally block the inhibitory effects of short days on neuroendocrine-gonadal activity. Communally-housed hamsters receiving a 10-second light pulse once every two, four, or seven days also exhibited paired testis and seminal vesicle weights, as well as serum gonadotropin levels, that were consistently higher than the values obtained for animals exposed only to LD 6:18.(ABSTRACT TRUNCATED AT 250 WORDS)

Timing of sexual maturity in female rhesus monkeys (Macaca mulatta) housed outdoors.

A comparison of the age and season at first parturition was made for spring-born female rhesus monkeys and for females born in the fall to mothers who had been laboratory-housed before being transferred outdoors. Females (N = 9) born during the fall had first parturition during the spring and summer, as did all spring-born females (N = 68), and not during the fall as would be predicted if age were the determining factor. A separate analysis of post-menarchial, spring-born females (N = 5) beginning in September at 29 months of age revealed that the ensuing 12 months were characterized by low serum levels of oestradiol (less than 50 pg/ml), progesterone (less than 1.0 ng/ml), LH (less than 7.0 ng/ml), and FSH (less than 5.50 micrograms/ml). First ovulation subsequently occurred in the fall in all subjects at a mean age of 41.9 +/- 0.1 months, and was preceded by significant elevations in basal LH and FSH, coincident in time with the transition of summer to fall (September). Female copulatory behaviour was restricted to the period surrounding first ovulation, beginning some 2 weeks before and ceasing within 3 days after the oestradiol peak. The most rapid gain in weight occurred during the summer months before first ovulation, and was associated with significant elevations in serum GH and prolactin. These data suggest that season may influence the timing of sexual maturation in rhesus monkeys kept outside in such a way that the occurrence of first ovulation is restricted to the fall and winter months.

The dark mink: a model of male infertility.

Breeding mink for a fine dark fur has coselected male infertility, which may be manifest at the onset of breeding (primary infertility) or after one or more fertile breeding seasons (secondary infertility). Mink with primary infertility have low LH and testosterone levels. However, they respond to exogenous GnRH with increases in LH production and in the number and size of LH and FSH positive gonadotropes in the anterior pituitary. Exogenous human CG also induces testosterone secretion. Thus, mink with primary infertility are probably defective in GnRH secretion, which is due either to abnormal hypothalamic function or its control mechanisms. Autoimmune orchitis with testicular immune complexes are frequent in mink with secondary infertility, suggesting an autoimmune etiology. In contrast, fertile dark mink and fertile mink with the opaline and pastel fur have normal serum LH and testosterone levels; their testes are also normal. In mink with secondary infertility, the frequency and degree of orchitis and testicular immune complexes increased from March (peak sexual activity) to April (onset of testicular regression). Thus, testicular autoimmunity most likely develops during testicular regression. Antisperm antibodies also increased in frequency during testicular regression in the fertile dark mink and in dark mink with primary and secondary infertility. Thus, antisperm antibody per se is insufficient to induce autoimmune orchitis. It is concluded that the infertile mink is a useful model of human male infertility, involving both endocrinological and immunological mechanisms.

Fertility after childbirth: changes in serum gonadotrophin levels in bottle and breast feeding women.

Changes in basal serum gonadotrophin levels during the resumption of ovarian activity post partum have been studied longitudinally in breast and bottle feeding mothers. On the basis of urinary steroid levels, ovarian activity was classified as showing complete suppression, follicular activity only, deficient luteal phases or normal menstrual cycles. Complete suppression of ovarian activity during lactation was associated with normal levels of FSH but low levels of LH. The resumption of follicular development was not accompanied by any increase in levels of either LH or FSH when compared with the phase of complete suppression and this pattern persisted during menstrual cycles characterized by deficient luteal phase progesterone secretion. Basal LH levels did not rise to normal levels during lactation until the resumption of normal ovulatory cycles. FSH secretion remained at a level comparable with the follicular phase of normal ovulatory cycles throughout the post partum period. In mothers who did not breast feed, LH levels rose more rapidly than in breast feeding mothers and had returned to within normal limits by three weeks post partum. At 4 weeks post partum FSH levels were lower in bottle feeding mothers than in breast feeders probably in response to the early rise in oestrogen levels among bottle feeders. These results suggest that decreased LH but not FSH secretion may be important in maintaining infertility associated with breast feeding.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of a new antiestrogen, keoxifene (LY156758), on growth of carcinogen-induced mammary tumors and on LH and prolactin levels

Keoxifene (LY156758) is a new benzothiophene-derived anti-estrogen with an extremely low degree of estrogenicity. Administration of 1–20 mg/kg per day inhibited the growth of 7, 12-dimethyl-benzanthracene (DMBA)-induced mammary tumors in rats. The degree of inhibition of mammary tumor growth was similar to that observed with tamoxifen treatment. In ovariectomized (OVX) rats daily treatment with 2 μg of estradiol benzoate resulted in low serum LH and prolactin levels in the morning followed by greatly elevated levels in the late afternoon. Keoxifene, but not tamoxifen, prevented the lowering of serum LH levels by estradiol in the morning, while tamoxifen, but not LY156758, blocked the afternoon elevation of serum LH. The afternoon increases in serum prolactin were antagonized to a greater extent by tamoxifen than by LY156758. The increase in uterine weight after estradiol benzoate was antagonized to a significantly greater extent with keoxifene than with tamoxifen, and in intact female rats keoxifene produced a significantly greater regression of the mammary gland than did tamoxifen. The results of this study indicate that keoxifene has a greater antiestrogenic effect than tamoxifen on estrogen target organs, but the greater degree of antiestrogenicity is not reflected in an enhanced antitumor effect. The lack of an enhanced antitumor effect may be the result of the lesser ability of keoxifene to antagonize the estradiol-induced surges of prolactin, or the partial estrogenic effects of tamoxifen may play a role in its anti-mammary tumor effects.

Gonadotropin responses to gonadotropin-releasing hormone and prolactin responses to thyrotropin-releasing hormone and metoclopramide in women with amenorrhea and insulin-treated diabetes mellitus.

Gonadotropin responses to GnRH and PRL responses to TRH and metoclopramide (MTC) were investigated in nine consecutive women with amenorrhea and insulin-treated diabetes mellitus. Nine normal menstruating diabetic women, 12 normal women in the early follicular phase, and nine consecutive nondiabetic women with functional amenorrhea served as controls. No significant differences were found in relation to diabetes regulation within the two diabetic groups. Amenorrheic patients with diabetes mellitus had significantly lower basal PRL levels than normal women and estradiol levels compared to the other groups. Basal plasma LH concentrations were significantly lower in women with amenorrhea and diabetes mellitus than in nondiabetics with amenorrhea, whereas plasma FSH levels were similar in all groups. The LH response to GnRH was significantly lower in amenorrheic patients with diabetes mellitus than in normal women, and a significant correlation (r = 0.81, P less than 0.01) was found between the LH response to GnRH and the basal estradiol level in these women. The FSH response to GnRH and the PRL response to TRH were similar in all groups. Amenorrheic diabetics had significantly lower PRL responses to MTC compared to other groups, and nondiabetics with amenorrhea had significantly lower PRL response than normal women. It is concluded that diabetic patients with functional amenorrhea have low basal and MTC-stimulated PRL levels, low basal LH levels, and decreased LH response to GnRH despite low estrogen levels. These hormonal changes may in part be caused by a raised central dopaminergic activity leading to a depression of pituitary ovulatory mechanisms.

Differential hypothalamic control of FSH secretion: A review

There are many circumstances in which the release of FSH and LH is dissociated; however, many of these are now thought to be brought about by interactions of LH-releasing hormone (LHRH), which stimulates not only LH but also FSH release, and the gonadal peptide, inhibin, which acts at the pituitary to suppress FSH release selectively. There are also many examples which can only be explained by postulating separate hypothalamic control of FSH and LH release. For example, electrochemical stimulation of the medial preoptic area elicited only LH release, whereas stimulation further caudally elicited equivalent LH release but FSH release as well. Points of stimulation particularly in the dorsal anterior hypothalamic area (DAHA) evoked only FSH release. Furthermore, implantation of prostaglandin E2 in various hypothalamic loci in a region extending from the DAHA caudally and ventrally to the caudal median eminence (ME) selectively elicited FSH release. Lesions of the DAHA resulted in a decrease of plasma FSH but not LH in castrated male and female rats and also suppressed the post-castration rise in FSH in males. In ovariectomized estrogen-primed rats with DAHA lesions, injection of progesterone provoked a normal LH surge but a significantly depressed FSH surge. Anterior ME lesions in castrates lowered LH levels more than FSH levels. Extracts of the DAHA evoked greater FSH and LH release in vitro than could be accounted for by the content of LHRH in the extracts, but there was no preferential release of FSH. On the other hand, extracts of the organum vasculosum lamina terminalis (OVLT) evoked dramatically increased FSH release above that which could be accounted for by the content of LHRH. Lastly, posterior ME extracts had more FSH-releasing activity than could be accounted for by their content of LHRH. All these results suggest the existence of an FSH-releasing factor (FSHRF) and lead to the speculation that the cell bodies of FSHRF neurons are located in the DAHA, with axons projecting to the OVLT and to the posterior ME. In other experiments, attempts were made to purify rat and sheep hypothalamic extracts by gel filtration on Sephadex G-25 and to assay the FSH-releasing activity by both bio- and immunoassay. Using this approach, we obtained evidence for the early emergence of a bioactive FSHRF prior to the emergence of LHRH from the column. Although much more work remains to be done, the accumulated evidence strongly supports the concept of a distinct FSHRF.

Inhibition of reproduction in rams by long daylengths and the acute effect of superior cervical ganglionectomy

Six castrated Soay rams were given testosterone implants, and exposed to an artificial lighting regimen of alternating 16-week periods of long days (16L:8D) and short days (8L:16D) for over 1 year. Under these conditions, the blood plasma concentration of testosterone was maintained relatively constant (4.3--6.4 ng/ml), while the levels of LH and prolactin varied in relation to the alterations in the photoperiod; low levels of LH occurred during long days when the rams were hyperprolactinaemic. During the last period of exposure to long days, 4 of the rams were cranially sympathectomized by removing the superior cervical ganglia. The effect of long daylengths on the secretion of LH and prolactin was blocked; prolactin concentrations began to decline after 2 weeks and LH levels increased. Ganglionectomy also influenced the plasma levels of melatonin; after the operation there was no longer a consistent 24-h rhythm in melatonin values and the increase associated with darkness was abolished. This results supports the view that the regulation of melatonin secretion is involved in the photoperiodic control of reproduction in rams.

Is the First or Second Periovulatory Surge of FSH Responsible for Follicular Recruitment in the Hamster?

AbstractProestrous hamsters were injected at 1300 hr with phenobarbital to block ovulation. The animals were bled via cardiac puncture every 6 hr beginning at 1600 hr of proestrus until 1000 hr of estrus. The ovaries were then removed and a quantitative evaluation of follicular development carried out. In saline-injected proestrous hamsters, there was a peak of serum FSH and LH at 1600 hr followed by a second prolonged peak of FSH at 0400 and 1000 hr of estrus accompanied by low tonic levels of LH. This hormone profile was associated at 1000 hr of estrus with an average of 9.3 large preantral follicles (stage IV follicles) per ovary. In contrast, the phenobarbital-treated hamsters showed no increases in either gonadotropin at any time and the ovaries contained large antral follicles and an average of only 1.7 stage IV follicles per ovary (three of four animals). Injection of 1 mg progesterone concurrent with phenobarbital restored the first surge of LH but not FSH and partially restored the second peak of...

Prolactin responsiveness to TRH and metoclopramide in thalassaemia.

SUMMARYPRL and gonadotrophin secretion has been evaluated in six prepubertal male thalassaemic patients and nine females. Four of the latter were sexually immature (group 1) and the remainder had more advanced sexual development (group 2). Subjects were challenged with LHRH (100 μg), TRH (200 ug) as well as the dopaminergic antagonist, metoclopramide (10 mg) and their responses compared with normal adult controls. The male patients had low testosterone, oestradiol and basal and peak LH responses to LHRH. FSH values were intact. Basal PRL levels, as well as PRL responses to TRH and metodopramide were normal. There was a further increase in PRL response to TRH after the administration of a long acting testosterone preparation. In group 1 females, basal and peak gonadotrophins and oestradiol were decreased. Basal PRL was normal, but there was a markedly impaired PRL response to both TRH and metoclopramide. Oestradiol valerate administration restored the impaired PRL response to TRH, but not to metoclopramide in group 1 female subjects, although conjugated oestrogens had no effect. Group 2 females had normal gonadotrophin profiles, but low oestradiol levels. Their PRL response to TRH was normal, but they also demonstrated an impaired PRL response to metoclopramide. It is concluded that the impaired PRL reserve in female thalassaemic patients could be due to iron infiltration in the pituitary, or to oestradiol deficiency. It may also be related to the low LH levels or, alternatively, it may represent some alteration in dopamine tone.

Peripheral blood and ovarian levels of sex steroids in the lactating rat.

Changes in progesterone (P), 20α-dihydroprogesterone (20α-OHP), testosterone (T) and estradiol-17β(E2) in peripheral blood, in corpora lutea (CL) of pregnancy and lactation and non-luteal ovarian tissues (NLO), and serum levels of LH, FSH and prolactin (PRL) were determined by radioimmunoassay in lactating rats nursing 8 pups. CL of pregnancy and lactation and NLO were removed at various days after post-partum ovulation (Day 0 of lactation=day of parturition).Serum E2 remained low until Day 10 of lactation followed by a slight increase from Days 12 to 21. Serum T was unchanged throughout lactation. Low levels of T and E2 in NLO were observed until Day 12, followed by a gradual increase on Day 15 and onward. These changes correlated with low levels of serum LH from Days 2 to 12 and a return to basal levels on Days 15 to 21. Throughout lactation serum FSH remained at basal levels corresponding to diestrous values during the estrous cycle. High levels of serum PRL were observed from Days 4 to 10. Serum levels of P reached maximal values between Days 8 and 10 and decreased after Day 12. Changes in serum 20α-OHP were inversely related to serum P throughout lactation. The CL of pregnancy contained large amounts of 20α-OHP and small amounts of P on Days 1 and 2 followed by an abrupt decline until Day 21. On the other hand, a marked increase in content and concentration of P in the CL of lactation occurred between Days 6 and 12 followed by a gradual decline by Day 21. Content and concentration of 20α-OHP in the CL of lactation increased progressively from Day 1 to 21.These findings indicate that the CL of pregnancy secrete a large amount of 20α-OHP and a small amount of P during the early stages of lactation. Thereafter, the CL of lactation markedly increase their ability to secrete P. High levels of P and PRL during the first half of lactation along with strong suckling stimuli may be involved in the suppression of follicular development, presumably by lowering basal levels of serum LH.

Reproductive hormone profiles in male anorexia nervosa before, during and after restoration of body weight to normal. A study of twelve patients

Twelve male subjects with anorexia nervosa have been studied in respect of various aspects of their hormonal status. Initially low plasma levels of testosterone and LH increase significantly as weight is regained to matched population mean levels. LH response to releasing hormone is absent at low body weight, enhanced at transitional early/mid-pubertal body weight and normal at newly restored adult body weight. It is claimed that these changes as experienced by the individuals concerned during weight gain must necessarily be taken into account in the attendant psychotherapy, and can then provide the opportunity for psychological growth and greater capacity this time to cope with the inevitably rekindied adolescent turmoil.

Influence of ingested petroleum on the reproductive performance and pituitary-gonadal axis of domestic ducks ( anas platyrhynchos)

1. The chronic ingestion of a sublethal dose (5%) of dietary North Sea crude oil delayed the onset of lay in adult Khaki Campbell ducks transferred from a short (8L:16D) to long day (16L:8D) photoperiod and greatly reduced the rate of oviposition and quality (weight and shell thickness) of the eggs subsequently laid. 2. Refeeding the oil-fed birds with the uncontaminated control diet stimulated the rate of egg production and improved egg quality, but in both cases not to the level in the controls. 3. Food intake and the plasma calcium level in the petroleum-fed birds were reduced, but these effects are unlikely to be causally responsible for the adverse effects of petroleum on avian reproduction. 4. Gonadotrophic (luteinizing hormone, LH) hormone secretion in the oil fed birds was not suppressed and the impairment of reproductive performance was not due to low plasma LH levels. 5. The reduced rate of lay in the oil-fed birds was accompanied by low gonadal steroid (progesterone) levels. The detrimental effects of oil on reproduction may be due to direct or indirect effects on the ovary or shell gland.

The effects of castration on the seasonal pattern of plasma LH concentrations in wild mallard drakes

Castration of photorefractory wild mallard drakes caused a significant increase in their plasma LH concentrations. Blood samples were then taken at monthly intervals for 16 months from 10 castrated drakes living outdoors in Kiel (54°N). Mean plasma LH levels remained elevated throughout the year. It is suggested that the testicular feedback is important for the maintenance of low LH levels during the refractory period, for the typical seasonal fluctuations of the plasma LH concentrations of intact birds, and probably for the induction of photorefractoriness.

A comparison of the responses of captive willow ptarmigan ( Lagopus lagopus lagopus), red grouse ( Lagopus lagopus scoticus), and hybrids to increasing daylengths with observations on the modifying effects of nutrition and crowding in red grouse

The photoperiodic responses of two races of Lagopus lagopus from different latitudes and of hybrids between them were compared under the same lighting conditions. The captive birds were descended from northern Norwegian willow ptarmigan ( Lagopus lagopus lagopus) and Scottish red grouse ( Lagopus lagopus scoticus). Under natural conditions, the red grouse begin to lay eggs 3 weeks earlier than the willow ptarmigan. Photosensitive birds were transferred from an 8-hr daylength to a lighting regime in which the daylength was increased by 1 hr per week for 11 weeks. At the start of the study, the red grouse had greater LH levels and comb sizes than the wilow ptarmigan or the hybrids. The critical daylength needed to stimulate LH secretion was less than 12 hr in both races but it was not clear whether it was greater in the willow ptarmigan than in the red grouse. However, the races differed quantitatively: the willow ptarmigan had lower LH levels at 12, 13, and 14-hr photoperiods than did the red grouse or the hybrids. In all the males, comb heights increased significantly ( P < 0.05) after the photoperiod was increased to 12 hr and reached their maximum in the red grouse, hybrids, and willow ptarmigan at photoperiods of 13, 14, and 16 hr, respectively. The female red grouse, hybrids, and willow ptarmigan laid their first eggs after the photoperiod was increased to 15, 17, and 19 hr, respectively. At the end of the study the red grouse but not the hybrids or willow ptarmigan were becoming photorefractory. A low-protein diet did not alter the timing of the onset of seasonal breeding in captive female red grouse although it did cause a reduction in the rate of lay and egg weight. The onset of seasonal breeding was delayed, however, when the birds were crowded. It was concluded that in L. lagopus, the photoperiodic response seems to be determined by inherited factors. Further, the absence of a clear difference between the critical daylengths in red grouse and willow ptarmigan raises the possibility that differences in the timing of the onset of seasonal breeding in these races may be caused by modifications in the neural or endocrine pathways “downstream” from the biological clock.

Pituitary function in idiopathic haemochromatosis: hormonal study in 36 male patients.

Thirty-six male patients with idiopathic haemochromatosis were subjected to measurements of basal plasma values of testosterone, LH and FSH and to an LRH test. Nineteen were also subjected to basal plasma determinations of T3, T4, cortisol, TSH and prolactin and to a TRH test. In 11 cases GH values were measured before, during and after an arginine infusion. Seventeen patients were found to hae low levels of testosterone, LH and FSH, and no gonadotrophin responses to LRH. Seventeen others had normal levels of these three hormones, with normal responses to LRH. The two remaining patients had normal testosterone values but very increased gonadotrophin values: a fact which remains unexplained. Basal levels of prolactin, GH, T3, T4, and TSH were normal: cortisol levels were either normal or increased in cases of poorly controlled diabetes. Prolactin responses to TRH were always normal. TSH responses to TRH were impaired in 2 cases, and GH responses to arginine in 3 cases. Considering that other factors may be involved in the few impairments found in TSH and GH stimulations, it is concluded that the only indisputable pituitary insufficiency in about half of the cases of idiopathic haemochromatosis is gonadotrophic.