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Biomedical subjects

F Petraglia

Publications and source records attributed to F Petraglia.

At least 289 records · Page 16Linked to original sources
PubMed1988

Steroid replacement treatment increases beta-endorphin and beta-lipotropin plasma levels in postmenopausal women.

The present study shows the effects of two different steroid replacement therapies, with conjugated estrogens or with a new synthetic steroid derivative, ORG OD14, on plasma beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) levels in postmenopausal subjects. Blood samples were collected before treatment and after 1, 2 and 4 months of treatment; a third group of patients was treated with placebo. After 2 months of treatment both groups of patients who underwent steroid supplementation showed circulating levels of beta-EP and beta-LPH higher than basal levels. ORG OD14 treatment increased beta-EP and beta-LPH levels more than conjugated estrogens at the 2nd month of therapy. No further change was found after 4 months. The two drugs were effective in reducing hot flushes and improving physical and psychological symptoms. These data indicate that sex steroids are able to increase beta-EP and beta-LPH secretion in postmenopausal women, with a concomitant relief of climacteric symptoms.

Adult↗
PubMed1988

Evidences for a dopamine-regulated peripheral source of circulating beta-endorphin.

Circulating beta-endorphin (beta EP) and beta-lipotropin (beta LPH) concentrations increase after the administration of acetylcholine or serotonin agonist drugs. In this study we examined the effect of dopamine receptor agonists and/or antagonists on plasma beta EP, beta LPH, cortisol, and PRL levels in normal subjects. Neither direct dopamine (DA) agonist drugs, DA (1 microgram/kg min for 120 min), bromocriptine (2.5 mg po), L-dopa (500 mg po) or an indirect DA agonist, nomifensine (200 mg po), significantly altered plasma beta EP and beta LPH levels. The administration of metoclopramide, a DA antagonist (10 mg iv), significantly increased plasma beta EP, beta LPH, PRL, and cortisol levels. This effect was completely reversed by pretreatment with L-dopa (500 mg po) and only partially antagonized by DA infusion. Domperidone (10 mg iv), a DA antagonist which does not cross the blood brain barrier, increased only plasma beta EP levels, an effect inhibited both by L-dopa and DA. After dexamethasone (2 mg/day for 2 days) domperidone still increased plasma beta EP and PRL levels. The concomitant increase of beta EP, beta LPH, and cortisol after metoclopramide suggests that endogenous DA inhibits the secretion of proopiomelanocortin-related peptides. Moreover, since domperidone increases only beta EP and this effect is not altered by dexamethasone, there may be a corticotropin-releasing hormone-independent source of circulating beta EP in humans, which is inhibited by DA.

Acetylcholine↗
PubMed1988

Impairment of the opioidergic control of luteinizing hormone secretion in Turner's syndrome: lack of effect of gonadal steroid therapy.

We studied the activity of endogenous opioid peptides in regulating LH secretion in patients with Turner's syndrome. To do so, we determined the LH secretory response to opiate receptor blockade by naloxone (0.08 mg/kg BW, iv) in 17 patients (age range, 9-23 yr). Eight patients were untreated (3 of whom had had spontaneous menarche), and 9 patients were taking ethinyl estradiol/medroxyprogesterone acetate treatment (5 of these patients were also studied before treatment). In addition, the plasma LH responses to GnRH (50 micrograms, iv) and placebo were determined in the patients as well as in 13 age-matched normal girls (6 prepubertal and 7 pubertal). Naloxone did not increase plasma LH levels in the amenorrheic untreated and treated patients with Turner's syndrome. However, in the 3 patients who had had spontaneous menarche and in normal pubertal girls naloxone increased plasma LH levels. GnRH was effective to the same extent in the patients and normal subjects. These results indicate that in patients with Turner's syndrome the opioidergic inhibition of LH secretion is impaired and is not restored by gonadal steroid replacement therapy. Moreover, the normal plasma LH responses to naloxone in the spontaneously menstruating patients with Turner's syndrome indicate both the clinical variability of this syndrome and the participation of endogenous opioid peptides in the regulation of normal menstrual function.

Adolescent↗
PubMed1988

Response of circulating adrenocorticotropin, beta-endorphin, beta-lipotropin and cortisol to athletic competition.

Acute physical exercise stimulates the activity of the hypothalamus-pituitary-adrenal axis in man. In the present study we measured plasma adrenocorticotropin, beta-endorphin, beta-lipotropin and cortisol levels in 27 male trained athletes in basal conditions, 60 min before and immediately after an official competition. The endocrine responses were evaluated in different groups of athletes participating in races (100 m, 1500 m, 10,000 m) or in the disc throw. The athletes competing for the runs showed a statistically significant increase in plasma adrenocorticotropin, beta-endorphin, beta-lipotropin and cortisol levels after the race (P less than 0.01), whereas the disc throwers showed no significant change in the hypothalamus-pituitary-adrenal axis hormones after the competition. The percent increase in plasma adrenocorticotropin, beta-endorphin, beta-lipotropin and cortisol was higher in the athletes who run 1500 m and 10,000 m than in those participating in the short distance race (100 m). The present results showed that plasma proopiomelanocortin-related peptides and cortisol levels increase in trained athletes following running competition and that this increase is related to the duration of the physical exercise.

Adrenocorticotropic Hormone↗
PubMed1988

Impaired beta-endorphin response to human corticotropin-releasing hormone in obese children.

In order to evaluate the secretion of beta-endorphin in obese children and adolescents, we measured plasma beta-endorphin, ACTH and cortisol levels before and following administration of CRH (1 microgram/kg). Fourteen normal weight and 22 obese subjects (weight excess ranging from 30 to 98%) were studied. Plasma hormone levels were measured by radioimmunoassay directly in plasma (cortisol, ACTH) and after silicic acid extraction and Sephadex G-75 column chromatography (beta-endorphin). Basal beta-endorphin levels in obese children were significantly higher than in controls (14.7 +/- 1.8 vs 6.0 +/- 0.6 pmol/l; mean +/- SEM). No differences were found in basal ACTH and cortisol levels. CRH administration significantly increased beta-endorphin, ACTH and cortisol levels in normal subjects and ACTH and cortisol levels in obese subjects. Plasma beta-endorphin levels in obese children and adolescents did not show any significant increment. These data confirm the higher than normal beta-endorphin plasma levels in obese subjects in childhood and demonstrate that CRH is unable to increase beta-endorphin levels, suggesting an impairment of the hypothalamo-pituitary control mechanisms or an extra-anterior pituitary source.

Adolescent↗
PubMed1988

Transient failure of central opioid tonus and premenstrual symptoms.

In order to evaluate the relationships between endogenous opioid activity and premenstrual complaints, we subjected three groups of patients in the mid (days 8-12 prior to menses) and late (days 1-5 prior to menses) luteal phases of the cycle to a naloxone test and some of the patients to a luteinizing-hormone-releasing hormone (LHRH) test. The premenstrual syndrome (PMS) group was composed of nine patients complaining of dizziness, irritability and depression close to menses for at least three years. The menstrually related migraine (MM) group was composed of 15 patients complaining of premenstrually related migraine. The common migraine (CM) group was made up of 16 women suffering from common migraine for years whose attacks occurred independently of menstrual cycle events. A group of seven fertile women served as controls. Every two days the patients filled out the Menstrual Distress Questionnaire for evaluation of their complaints. After the evaluation of spontaneous LH pulsatility for one hour, 4 mg of naloxone was injected as a bolus, and samples were collected every 15 minutes for 2 hours. Both estradiol (E2) and progesterone (P) were measured in basal samples from each naloxone test. LH responsiveness to LHRH was similar in the mid and late luteal phases and did not change between groups. In the mid luteal phase the LH response to naloxone in PMS and MM patients was similar to that in normal subjects, while CM patients had impaired LH secretion. In the premenstrual phase only the controls maintained an LH responsiveness similar to that observed in the mid luteal phase, while both PMS and MM lost the naloxone-induced LH release.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Beta-lipotropin is the major component of the plasma opioid response to surgical stress in humans.

There is growing experimental evidence that beta-endorphin immunoreactivity is raised by surgical stress in patients undergoing general anesthesia. As the assay methods employed to date did not allow to fully discriminate between beta-endorphin and its immediate precursor, beta-lipotropin, we have investigated in the present study plasma levels of these two peptides by separating them by chromatography on plasma extracts prior to radioimmunoassay in eighteen surgical patients under general anesthesia and eight under spinal anesthesia. Beta-lipotropin, but not beta-endorphin, plasma levels were found to be significantly elevated during surgery in the general anesthesia group, while no change was found in either peptide concentration in the spinal one. Cortisol plasma levels also increased significantly 90 minutes after the beginning of surgery, when they were positively correlated to beta-lipotropin ones. Although the sampling time we adopted may have prevented us from detecting an early peak of beta-endorphin during the first 30 minutes of surgery, the major component of the pituitary opioid response to surgical stress appears to be related to beta-lipotropin. This is in agreement with results of experimental work on various kinds of stress in animals and humans and seems to rule out a role for plasma beta-endorphin in post-operative analgesia.

Adult↗
PubMed1987

Localization, secretion, and action of inhibin in human placenta.

Inhibin is a gonadal glycoprotein hormone that regulates the production of follicle-stimulating hormone (FSH) by the anterior pituitary gland and exhibits intragonadal actions as well. The present study shows that inhibin-like immunoreactivity (inhibin-LI) is present in cells of the cytotrophoblast layer of human placenta at term and in primary cultures of human trophoblasts. Human chorionic gonadotropin (hCG) stimulated secretion of inhibin-LI from these cultured placental cells. This effect was mimicked by 8-bromo-cyclic adenosine monophosphate (8-bromo-cAMP), forskolin, and cholera toxin, suggesting that the mechanism of hCG induction of placental inhibin-LI secretion is cAMP-dependent. Incubation with an antiserum that binds the alpha-subunit of human inhibin increased the secretion of hCG and gonadotropin-releasing hormone-like immunoreactivity (GnRH-LI) from trophoblast cells in culture, suggesting a local tonic inhibitory action of endogenous inhibin on hCG and GnRH-LI release. The action of inhibin on hCG secretion may partially require the presence of placental GnRH, as suggested by evidence that a synthetic GnRH antagonist partially reverses the hCG increase induced by inhibin immunoneutralization. Results suggest paracrine roles for both inhibin and GnRH in the regulation of placental hCG production.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1987

No gradient exists between lumbar and ventricular cerebrospinal fluid beta-endorphin.

In 8 patients, beta-lipotropin (beta-LPH), beta-endorphin (beta-EP), ACTH, protein and chloride concentrations were measured in cerebrospinal fluid (CSF) samples obtained simultaneously from the lumbar space and lateral ventricle. Albumin and IgG levels were significantly higher in lumbar than in ventricular CSF samples while no craniocaudal gradient was observed for neuropeptide concentrations. The importance of molecular weight in determining such a regional distribution is supported also by the similar lumbar and ventricular levels of chlorides. These data would validate the CSF approach through lumbar puncture as a tool for exploring neuropeptides in the central nervous system.

Adrenocorticotropic Hormone↗
PubMed1987

Feed-back effect of growth hormone on hypothalamic opioid and somatocrinin producing neurons.

Reportedly, most acromegalics are refractory to the growth hormone (GH)-releasing effect of central nervous system-acting stimuli. For instance, the synthetic analogue of met-enkephalin (Enk) viz. FK 33-824 fails to alter the high circulating GH levels of acromegalics. The most likely interpretation of such finding is that circulating GH disrupts, for a negative feedback effect, hypothalamic opioid function and/or GH-releasing hormone (GHRH) producing neurons, through which opioids exert their action. To address this issue, we have evaluated in intact and hypophysectomized male rats the effect of a high-dose GH regimen on the hypothalamic stores of endogenous opioid peptides, beta-endorphin (beta-EP) and met-enkephalin (met-enk). Moreover we have evaluated in intact male rats the effect of exogenous GH on median eminence (ME) GHRH stores and the ability of FK 33-824 to stimulate GH and prolactin (PRL) secretion and of exogenous GHRH to induce GH secretion. Human GH (25 and 250 micrograms bid for 4 days) administered to hypophysectomized rats strikingly reduced beta-EP and met-enk-like immunoreactivity (LI) in the medial basal hypothalamus, the effect being already maximal with the lower hGH dose. The higher dose of hGH diminished, though to a lower extent, hypothalamic beta EP-LI content also in intact rats, and reduced GHRH-LI content in the ME. Despite these profound biochemical alterations, the GH responsiveness to GHRH and FK 33-824 administration was preserved, while the latter drug induced a lower PRL rise in GH-treated than in control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Ontogeny of pituitary beta-endorphin and related peptides in the human embryo and fetus.

In this study we evaluated the presence of proopiomelanocortin-related peptides (beta-lipotropin, beta-endorphin, and gamma-endorphin) in five embryos (5 to 10 weeks of pregnancy) and 11 fetal pituitaries (15 to 25 weeks) by means of high-performance liquid chromatography coupled with specific radioimmunoassays. Tissues were collected at laparotomy for ectopic pregnancy (five embryos) or after spontaneous (seven) or prostaglandin-induced (four) abortion. beta-Endorphin and beta-lipotropin were present starting at the seventh week of pregnancy while gamma-endorphin appeared only in the second trimester. During embryonic life opioid activity was limited to the cephalic portion. The three peptides, but little, if any, acetylated 1-31 beta-endorphin, were recognized in the fetal pituitary throughout the second trimester, at which time beta-lipotropin and beta-endorphin showed constant values in spite of increasing gamma-endorphin concentrations. beta-Lipotropin was the predominant peptide in both embryonic and fetal life. In conclusion, the three peptides related to proopiomelanocortin were expressed from the precursor at different times throughout development. By the beginning of the second trimester the pituitary processing of proopiomelanocortin is similar to that of adult life and the functional activity of the anterior lobe seems to prevail over that of the "fetus-related" neurointermediate lobe around the twenty-fifth week of pregnancy.

Chromatography, High Pressure Liquid↗
PubMed1987

Effects of Org OD 14 on pituitary and peripheral beta-endorphin in castrated rats and post-menopausal women.

The aim of the first part of this study was to evaluate the effects of a new synthetic steroid (7 alpha,17 alpha)-17-hydroxy-7-methyl-19-norpregn-5(10)-en-20-yn-3-one (Org OD 14), on anterior pituitary (AP) and neurointermediate pituitary lobe (NIL) contents and on circulating levels of beta-endorphin (beta-EP) in rats. Three weeks after ovariectomy, groups of 9 rats were treated with either Org OD 14 (2 or 10 micrograms/day/rat for 14 days) or a placebo. In addition, 2 groups of ovariectomized rats were also treated with oestradiol benzoate (EB) (2 or 10 micrograms/day/rat for 14 days) to compare the effectiveness of the new steroid with that of a classical oestrogenic substance. beta-Ep concentrations were measured in plasma and in AP and NIL extracts by means of double-antibody radioimmunoassay (RIA), employing a specific anti-camel beta-EP (C-terminal fragment). Both doses of Org OD 14 induced a significant dose-related increase in plasma and pituitary lobe beta-EP concentrations as compared with the results on placebo treatment. By comparison, EB was active only at a dose of 10 micrograms/day. Despite the common stimulatory effects of EB and Org OD 14 on pituitary beta-EP, these findings suggest that the two steroids have different modes of action. The second part of the study investigated the changes in beta-EP and beta-lipotrophin (beta-LPH) plasma levels in a group of post-menopausal women treated for 6 months with Org OD 14 (2.5 mg/day) in comparison with the levels in a placebo-treated group. The clinical efficacy of Org OD 14 treatment in post-menopausal symptoms was confirmed, as well as its lack of or only transient effect on plasma lipids and lipoproteins. beta-EP and beta-LPH plasma levels were significantly higher in the Org OD 14-treated group than in the placebo group as from the second month until the end of the observation period.

Adult↗
PubMed1987

Proopiomelanocortin-related peptides and methionine enkephalin in human follicular fluid: changes during the menstrual cycle.

Several studies indicate the presence of different pituitary hormones or neuropeptides in ovarian follicular fluid from various species. Recently our group showed that the ovarian follicular fluid of health women contains two of the endogenous opioid peptides, beta-endorphin and methionine enkephalin, in concentrations that are tenfold to twentyfold higher than in circulating plasma. The presence of immunoreactive beta-lipotropin was also shown. The aim of the present study was to evaluate whether adrenocorticotropic hormone, which in pituitary cells is synthesized from proopiomelanocortin such as beta-endorphin and beta-lipotropin, is also present in follicular fluid and the possible changes of proopiomelanocortin-related peptides during the menstrual cycle. Concentrations of beta-endorphin, methionine enkephalin, adrenocorticotropic hormone, and beta-lipotropin were measured in 60 healthy menstruating women at different periods of the menstrual cycle (20 during the follicular, 22 in the preovulatory days, and 18 during the luteal phase). Thirteen women participated in an in vitro fertilization program and thus received clomiphene citrate (100 mg/day from the fifth to the ninth day) plus 5000 IU human chorionic gonadotropin before starting the program. All samples were collected at laparoscopy under general anesthesia. In another eight patients fluid was collected from follicular cysts. Peptides were extracted on octadodecasilyl silica columns with 80% methanol in 0.5 mol/L acetic acid. The identity of follicular fluid beta-endorphin, methionine enkephalin, adrenocorticotropic hormone, and beta-lipotropin and standard peptides was demonstrated with high-pressure liquid chromatography. Peptide concentrations were measured in extracts by radioimmunoassays either directly by (methionine enkephalin and adrenocorticotropic hormone) or after (beta-endorphin and beta-lipotropin) gel filtration on Sephadex G-75. The concentrations of methionine enkephalin, adrenocorticotropic hormone, and beta-lipotropin were similar in the different periods of the cycle. Conversely, beta-endorphin concentrations were significantly higher in preovulatory days than in the other periods; no differences were evident between spontaneous and stimulated cycles. These results indicate that proopiomelanocortin-related peptides are present in the follicular fluid and that beta-endorphin concentrations change during the menstrual cycle, with the highest values occurring in the preovulatory follicle.

Adrenocorticotropic Hormone↗
PubMed1987

Premenstrual fall of plasma beta-endorphin in patients with premenstrual syndrome.

Plasma beta-endorphin (beta-EP), beta-lipotropin (beta-LPH), and cortisol concentrations were measured by perimenstrual period in 11 patients affected by premenstrual syndrome (PMS) and in 8 asymptomatic healthy volunteers. Blood samples were collected every 2 to 3 days, for 1 month, starting from midcycle. The Menstrual Distress Questionnaire (MDQ) was administered during the testing period. Plasma beta-LPH and cortisol levels remain stable during the perimenstrual period, in both controls and PMS patients. On the contrary, PMS patients showed a decrease of plasma beta-EP in the week preceding menses and during the first days of menstrual flow. Beta-EP values of PMS patients regain normal levels during the next follicular phase. No changes of beta-EP levels were recorded in asymptomatic women. MDQ scores revealed that PMS patients complained of water retention, pain discomfort, and mood swings. The transient and reversible decrease of plasma beta-EP in PMS patients near to and at menses remains to be clarified.

Adult↗