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Biomedical subjects

M E Quigley

Publications and source records attributed to M E Quigley.

At least 37 records · Page 2Linked to original sources
PubMed1983

Acute suppression of circulating testosterone levels by cortisol in men.

The effect of acute activation of the ACTH-adrenal axis on circulating testosterone (T) levels was investigated. Elevation of circulating cortisol resulting from insulin-induced hypoglycemia or the administration of hydrocortisone was followed by a rapid decrease in serum T levels, without accompanying changes in LH or PRL. These findings suggest that hypercortisolism of endogenous or exogenous sources suppresses T secretion by a direct action on the testis. This adrenal-testicular axis may have biological implications on the reproductive adaptation to stress.

Adult↗
PubMed1983

Effects of tyrosine and tryptophan ingestion on plasma catecholamine and 3,4-dihydroxyphenylacetic acid concentrations.

The effect of oral tyrosine or tryptophan ingestion on plasma concentrations of norepinephrine (NE), dopamine (DA), epinephrine (EPI), and 3,4-dihydroxyphenylacetic acid (DOPAC) was investigated in a double blind, placebo-controlled study in fasted men. Tyrosine ingestion induced within 45 min a significant but short-lasting (approximately 30 min) increase in plasma concentrations of NE, EPI, and DA and a coincident decrease in plasma DOPAC levels. Ingestion of tryptophan or lactose placebo did not after plasma DA, EPI, NE, or DOPAC levels. Since plasma catecholamines derive from peripheral sources, while circulating DOPAC may reflect both brain and peripheral DA turnover, these results suggest that the oral ingestion of tyrosine can exert acute effects on catecholamine systems within and outside the brain.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1983

Hormonal dynamics at midcycle: a reevaluation.

The dynamics of ovarian and pituitary hormone changes during the midcycle period were evaluated. Changes in hormone levels were determined at 2-h intervals for 5 consecutive days during the periovulatory phase of the cycle in five women. During the 50 h preceding the onset of the surge, the rates of increments for estradiol (E2), progesterone (P4), and LH were similar, with doubling times of 57-61 h. The onset of LH and FSH surges was found to occur abruptly (LH doubled within 2 h). They were temporally associated with the attainment of peak E2 levels and occurred 12 h after the initiation of a rapid rise of P4. The mean duration of the surge was 48 h, with a rapidly ascending limb (doubling time, 5.2 h) lasting 14 h accompanied by a rapid decline of E2 and a continued rise of P4. The surge was followed by a peak plateau of gonadotropin levels lasting for 14 h and a transient leveling of P4. The longer descending limb (half-time, 9.6 h), lasting for 20 h, was associated with a second rapid rise of P4, beginning 36 h after surge onset or 12 h before termination of the surge. By using the onset of the LH surge as a reference point, our data provide a relatively precise picture of the hormonal changes preceding the onset of the gonadotropin surge and the temporal relationship between the multiphasic P4 rise and pituitary-ovarian function.

Androstenedione↗
PubMed1983

The disappearance of opioidergic regulation of gonadotropin secretion in postmenopausal women.

In postmenopausal women, the administration of beta-endorphin in repeated pulses (1-2.5 mg) at 1- to 2-h intervals or constant infusion (1 mg/h) for 3-6 h elicited the prompt release of PRL without concomitant change in LH levels. Infusion of an opiate receptor antagonist, naloxone (1.6 mg/h), for 6-7 h also had no effect on LH levels. Since substantial evidence indicates that endogneous opioid peptides exert an inhibitory role on GnRH-LH secretion and that the functional activity of opiate receptors appears to be ovarian steroid dependent, the present observation suggests that the hypersecretion of gonadotropin in the absence of ovarian steroid feedback may, in part, be causally related to a reduced opioid inhibition of GnRH-LH release.

Endorphins↗
PubMed1983

Pituitary hormone release in response to food ingestion: evidence for neuroendocrine signals from gut to brain.

The synchrony of PRL and cortisol release with feeding is now well established. To delineate further the neuroendocrine mechanisms involved, meal-related pituitary and adrenal cortical activities were investigated in seven normal men in a series of experiments conducted in random sequence at 1-week intervals. Ingestion of a standardized mixed meal elicited a consistent acute release of PRL and cortisol at noon (1200 h), but not at breakfast (0800 h). No measurable changes in other pituitary hormones were observed. The relative magnitudes of PRL and cortisol release in response to lunch were not significantly influenced by a preceding breakfast. These responses appear unrelated to the cephalic or oral phases of food ingestion. However, the composition of the meals was found to be important. Whereas carbohydrate meals had no discernible effects, high protein meals induced a large increase in both PRL and cortisol; high fat meals caused selective release of PRL. Ingestion of L-tyrosine and L-tryptophan induced remarkable increments in serum concentrations of both PRL and cortisol, suggesting that these essential amino acids may be active components of the high protein meal. Choline had no effect. Meal-mediated PRL and cortisol release was unaffected by prior receptor blockade of the opioidergic and cholinergic systems with naloxone and atropine, respectively. These observations indicate that the protein component of the meal was responsible for the midday surges of PRL and cortisol and that the cephalic-vagal pathway was not required in food-entrained pituitary hormone release. Further, our data suggest that the neurotransmitter substrates in the protein meal may serve to link the gut and brain by modifying central catecholamine and serotonin biosynthesis, and thereby influence the hypothalamic factors controlling pituitary PRL and ACTH secretion. The possibility that gastrointestinal hormones may also influence the hypothalamic-pituitary system remains to be explored.

Adult↗
PubMed1982

The food-entrained prolactin and cortisol release in late pregnancy and prolactinoma patients.

Abrupt and concomitant increments in circulating cortisol and PRL levels in association with food intake at noon were observed in hyperprolactinemic pregnant women. During late pregnancy, the quantitative release was at least 12-fold greater for PRL and substantially more for cortisol compared to values in nonpregnant women. In contrast, patients with hyperprolactinemia due to prolactinoma exhibited an absence of the PRL response to the noon meal and a significantly smaller rise in cortisol, suggesting an independent mechanism for the release of these two hormones due to food ingestion. These observations may be important for future elucidation of neuroendocrine links between feeding and metabolic homoeostasis in pregnancy.

Adenoma↗
PubMed1981

Increased luteinizing hormone sensitivity to dopamine inhibition in polycystic ovary syndrome.

The elevated LH secretion in 8 patients with the polycystic ovarian syndrome (PCO) was promptly suppressed by the infusion of dopamine (DA; 4 microgram/kg.min for 4 h). Compared to normal women studied during the early follicular phase, the maximal LH suppression due to DA infusion was significantly greater in PCO patients when expressed as either the net or percent decrease. This enhanced LH sensitivity to DA inhibition in PCO patients with chronically elevated estrogens, suggests that the inappropriately elevated LH release and the exaggerated LH pulses may be causally related, in part, to a reduction of endogenous DA inhibition of LH secretory activity.

Dopamine↗
PubMed1981

Endogenous opiates modulate pulsatile luteinizing hormone release in humans.

To test the postulate that endogenous opioid peptides may be involved in the neuroendocrine mechanisms controlling the frequency and amplitude of LH pulses, saline and an opioid receptor antagonist, naloxone, were infused sequentially, each for 6-h intervals, in six normal cycling women during the luteal phase of the menstrual cycle. During naloxone infusion (1.6 mg/h), there was a significant (P less than 0.01) increase in both the frequency and amplitude of LH pulses compared to those in saline controls. FSH pulses were not discernible in individual subjects; however, a significant increment in FSH levels occurred concomitantly with the increase in LH. These data strongly suggest that endogenous opiates, through an inhibition of hypothalamic LRF, participate in the endocrine events leading to the low frequency of episodic LH secretion characteristic of the luteal phase of the human menstrual cycle.

Adult↗
PubMed1981

Circadian rhythm in circulating concentration of dihydroxyphenylacetic acid in normal women.

The 24-h patterns of plasma concentration change in dopamine (DA) and its immediate deaminated metabolite, dihydroxyphenylacetic acid (DOPAC), were determined in 6 normal women (16 studies) by a modified radioenzymatic assay. Changes in DOPAC levels exhibited a marked circadian rhythm, with peak during the day and a nadir at night. At 1200 h, the DOPAC concentration increased significantly (P less than 10(-4)) to a peak value 62.9 +/- 8.4 ng/ml) 117% higher than the 24-h mean. At 2200 h, plasma DOPAC decreased (P less than 10(-4)) to a nadir concentration (10.0 +/- 3.3 ng/ml) 66% lower than the 24-h mean. The circadian rhythm of DOPAC could be reproducibly demonstrated over at least 4 successive days in individual subjects. There were no well defined circadian variations in plasma concentrations of DA. Since the plasma DOPAC concentration appears to reflect central nervous system dopaminergic neuronal activity, the present demonstration of a circadian rhythm of plasma DOPAC suggests that the activity of central nervous system DA-containing cells is higher during the day than at night.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1981

Acute prolactin release triggered by feeding.

An abrupt increment in serum prolactin (PRL) levels was demonstrated within 45 minutes of initiation of lunch at 1200 or 1400 h and supper at 1700 h. These observations establish that feeding triggers an acute release of PRL by the hypothalamic-pituitary unit.

Adult↗
PubMed1980

Evidence for increased dopaminergic inhibition of secretion of thyroid-stimulating hormone in hyperprolactinemic patients with pituitary microadenoma.

The administration of a dopamine-receptor antagonist, metoclopramide (10 mg, intravenous bolus), elicited a significant increase in the circulating concentration of thyroid-stimulating hormone (TSH) which was substantially greater for hyperprolactinemic patients with pituitary microadenoma than for normal women during the early follicular phase of the cycle. This study provides evidence of an inhibitory role of hypothalamic dopamine in the regulation of secretion of TSH and suggests an increased dopaminergic inhibition of secretion of TSH in these patients with prolactin-secreting tumors.

Adenoma↗
PubMed1980

Changes in pituitary hormones during and following transsphenoidal removal of prolactinomas.

Prolactin (PRL) and other pituitary hormones (luteinizing hormone, follicle-stimulating hormone, growth hormone [GH], thyrotropin stimulating hormone) were measured before, during, and after transphenoidal pituitary adenomectomy in 16 patients with hyperprolactinemia. The diagnosis of prolactinoma was made in three of the 16 patients by the absence of PRL response to thyrotropin-releasing factor (TRF) and a dopamine receptor antagonist, metoclopramide, without radiologic evidence of an adenoma. Contrary to findings in subjects with normal PRL values, the PRL rise in response to anesthesia and operation was absent. Other pituitary hormones, with the exception of GH, which increased during anesthesia and operation, exhibited no acute changes. In 11 of 16 cases, complete tumor removal was achieved as determined by the rapid decline of PRL levels to normal values within 24 to 48 hours after operation and by subsequent clinical follow-up. This finding documents that the adenoma is the main source of excessive PRL secretion. The circulating half time of immunoreactive PRL determined by frequent sampling in these patients was variable, ranging from 74 to 190 minutes, significantly longer than the previously reported value of 15 minutes determined by bioassay. Although a transient decline was evident, serum PRL levels remained elevated in those patients with incomplete tumor removal. These findings suggest that a single measurement of serum PRL within 24 to 48 following transphenoidal adenomectomy is a reliable indicator of the success or failure of the procedure.

Adenoma↗
PubMed1980

Evidence for an increased opioid inhibition of luteinizing hormone secretion in hyperprolactinemic patients with pituitary microadenoma.

The inhibiting role of endogenous opioid peptides on gonadotropin secretion was evaluated by the infusion of an opioid receptor antagonist, naloxone (1.6 mg/h for 4 h), in 10 hyperprolactinemic patients with pituitary microadenoma (prolactinoma) and 5 normal women during the early follicular phase of the cycle. In normal women, naloxone infusion induced no significant changes in any of the three pituitary hormones measured. Six prolactinoma patients with low normal levels of basal LH [10.0 +/- 1.0 mIU/ml +/- SE)] responded to naloxone infusion with an increment of circulating LH in the form of an amplified pulsatile pattern of release, which lasted for at least 2 h after the infusion. The other 4 patients with prepubertal levels of LH (4.9 +/- 0.8 mIU/ml) exhibited no LH response to naloxone. There were no significant changes in FSH or PRL levels in either group of patients. These findings suggest that an increased endogenous opioid inhibition of LH release occurs in patients with PRL-producing microadenoma.

Adenoma↗
PubMed1980

The role of endogenous opiates in LH secretion during the menstrual cycle.

To determine whether endogenous opiates exert an inhibitory action on LH secretion during the menstrual cycle, LH increments were examined in response to a specific opiate antagonist, naloxone, infused at 1.6 mg/hr for 4 hrs. Naloxone had no discernible effect on LH release during the early follicular phase. By contrast, a significant LH increment was observed in both the late follicular and mid-luteal phases of the cycle but the patterns of LH increment were distinct. Late follicular subjects exhibited slow, progressive increases in LH, while prompt, episodic and quantitatively greater LH increments were evident in mid-luteal phase subjects. These observations suggest that endogenous opiates are involved in the regulation of LH secretion during the high estrogen and estrogen-progesterone phases of the menstrual cycle.

Endorphins↗