Biomedical subjects

V Coiro

Publications and source records attributed to V Coiro.

At least 109 records · Page 6Linked to original sources

PubMed1992

Abnormal growth hormone and cortisol, but not thyroid-stimulating hormone, responses to an intravenous glucose tolerance test in normal-weight, bulimic women.

Abnormal growth hormone (GH) and adrenocorticotropic hormone (ACTH)/cortisol secretory patterns in response to a glucose load have been observed in underweight anorectic women. The present study was performed in an attempt to establish whether changes in the hypothalamic/pituitary sensitivity to hyperglycemia occur in bulimia in the absence of weight disturbance. Therefore, serum GH, plasma cortisol, and plasma insulin concentrations were measured in eight women with normal weight bulimia and in eight normal women during an intravenous glucose (0.33 g/kg as an IV bolus) tolerance test (IGTT). In addition, since abnormal pituitary hormone responses to a glucose load might reflect alterations in somatostatin (SRIH) release, TSH secretion also was measured, in view of its sensitivity to SRIH inhibition. Both GH and cortisol levels progressively and significantly declined during IGTT in the normal subjects. In the bulimic women, cortisol levels remained unchanged, whereas GH concentrations rose significantly after glucose injection. Plasma cortisol and serum GH levels were significantly higher in the bulimic than in the control subjects. No significant differences between groups were observed in hyperglycemia-induced insulin increments or in TSH decrements. These data indicate that an altered sensitivity to hyperglycemia affects the hypothalamic/pituitary centers controlling the secretion of the counterregulatory hormones GH and ACTH/cortisol in bulimia nervosa. The lack of a simultaneous change in the TSH secretory pattern argues against a possible involvement of SRIH in the pathophysiology of this disorder.

Adult↗

PubMed1992

Different effects of baclofen on LH and cortisol responses to naloxone in normal men.

The possible involvement of GABAergic B receptors in the control of LH and ACTH/cortisol secretion in response to naloxone was evaluated in seven normal men. Subjects were tested with naloxone (4 mg IV bolus plus 10 mg infused over 2 hr) with or without previous treatment with the gamma-aminobutyric acid (GABA)-ergic B receptor agonist, baclofen (5, 10 or 15 mg PO 30 min before naloxone). In additional experiments, six normal men were tested with 15 mg baclofen or placebo 30 min before a 2-hr infusion of normal saline. Plasma cortisol levels rose 70% in response to naloxone. The naloxone-induced cortisol rise was not modified by pretreatment with baclofen (5, 10 or 15 mg). Plasma LH concentrations rose 66% in response to naloxone. When the lowest dose of baclofen (5 mg) was administered, the LH response to naloxone remained unchanged. In contrast, 10 mg baclofen produced a significant reduction, and 15 mg baclofen completely abolished the naloxone-induced LH rise. The administration of baclofen or placebo alone did not change basal plasma levels of cortisol and LH. These data suggest that, in normal men, GABA B receptors participate in the endogenous opioidergic control of LH secretion, but not of ACTH/cortisol secretion.

Adrenocorticotropic Hormone↗

PubMed1992

Hypoglycemia-induced arginine vasopressin and oxytocin release is mediated by glucoreceptors located inside the blood-brain barrier.

Arginine vasopressin (AVP) and oxytocin (OT) responses during an insulin (0.15 IU/kg body weight) tolerance test (ITT) were evaluated in normal men while they were infused with normal saline, glucose or fructose. Insulin-induced hypoglycemia produced significant plasma AVP and OT increments in the control test. The infusion of fructose was unable to change the posterior pituitary hormonal responses to hypoglycemia. In contrast, AVP and OT responses during ITT were completely abolished when the concomitant infusion of glucose prevented insulin-induced hypoglycemia. These data exclude a direct role of hyperinsulinemia in the mechanism underlying the AVP and OT responses during ITT. Furthermore, since glucose, but not fructose, crosses the blood-brain barrier (BBB), the posterior pituitary hormone responses to hypoglycemia appear to be generated by stimulations of glucosensitive areas located inside the BBB.

Adult↗

PubMed1992

Stimulation of ACTH/cortisol by intravenously infused substance P in normal men: inhibition by sodium valproate.

The effect of synthetic substance P (SP), infused intravenously in doses of 0.5, 1 or 1.5 pmol/kg-1/min-1 over 60 min on ACTH/cortisol secretion was evaluated in 7 healthy men. SP tests and a control test with normal saline were randomly performed at weekly intervals. During tests, SP infusion did not produce untoward side effects or changes in blood pressure. Plasma ACTH and cortisol levels were not modified when normal saline or the lowest dose of SP were infused, whereas they were significantly increased in a dose-dependent fashion when higher amounts of SP were administered. Further studies were performed in another 7 healthy men to test the possible influence of GABAergic neurotransmission on the ACTH/cortisol response to SP. For this purpose, subjects were tested with SP (1.5 pmol/kg-1/min-1) alone and on a different occasion with SP after pretreatment with the GABAergic agent sodium valproate (200 mg 16, 8 and 1 h before the SP test). Again, the administration of SP induced a significant increase in plasma ACTH and cortisol levels. The pretreatment with sodium valproate completely abolished both ACTH and cortisol responses to SP. These data demonstrate for the first time in humans that the systemic infusion of SP stimulates ACTH/cortisol secretion, suggesting the involvement of a GABAergic mechanism in the regulation of the action of SP.

Adrenocorticotropic Hormone↗

PubMed1992

Diurnal variations in plasma ACTH, cortisol and beta-endorphin levels in cocaine addicts.

In order to establish possible alterations in the hypothalamic pituitary-adrenal axis and in ACTH-related opioids in cocaine addicts, plasma ACTH, cortisol and beta-endorphin levels were measured throughout the day in 9 cocaine addicts [age: 27 +/- 5 years (mean +/- SE); weight: 72 +/- 6.1 kg, duration of cocaine addiction: at least 2 years] on the day of their admission to a recovery community for drug abusers (first test) and after 15 days of abstinence (second test). Nine normal controls (age: 28 +/- 6 years; weight: 73 +/- 3.2 kg) were tested only once in a similar manner. Blood samples were taken at 06:00, 08:00, 10:00, 12:00, 18:00 and 20:00 h and served for hormonal assays. Urine samples were taken from cocaine addicts at 08:00 h on the experimental day and on the following day. Results of both urine assays were positive for cocaine catabolites, indicating cocaine administration during the day before the experimental test. From the day of their admission in the community (1st experimental day), the patients were forbidden to use cocaine. For 4 days after admission, they were treated with symptomatics to attenuate withdrawal symptoms. Thereafter, the patients underwent a washout period of pharmacological treatments for 10 days before being retested (second test). Urine samples taken at 08:00 h on this second experimental day and on the next day were negative for the presence of drug catabolites. During the first test, cocaine addicts showed higher plasma ACTH, cortisol and beta-endorphin levels than normal controls at all examined time points.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1992

Effect of potentiation of cholinergic tone by pyridostigmine on the GH response to GHRH in elderly men.

The plasma GH response to GHRH (100 micrograms i.v.) was evaluated either alone or after pretreatment with pyridostigmine (120 mg orally 1 h prior to GHRH) in 9 younger men (age range: 22-39 years) and in 9 healthy elderly men (age range: 63-77 years). On a different occasion, subjects were tested with pyridostigmine alone. Basal concentrations of glucose, cortisol, androgens, estrogens, thyroid hormones and GH were similar in all subjects, whereas insulin-like growth factor was lower in elderly men. The GH response to GHRH was significantly lower in the older (mean peak was 6 times higher than baseline) than in the younger group (mean peak was 11.3 times higher than baseline). The pretreatment with pyridostigmine induced a striking increase in the GH response to GHRH in the younger subjects (mean peak was 26 times higher than baseline), whereas it produced only a slight increase in the GHRH-induced GH response in elderly men (mean peak was 8.7 times higher than baseline). When pyridostigmine was given alone, plasma GH levels rose significantly in both groups; however, the pyridostigmine-stimulated GH response was significantly higher in younger (mean peak was 6 times higher than baseline) than in older subjects (mean peak was 2.5 times higher than baseline). These data indicate that the cholinergic stimulatory regulation of GH release is reduced in elderly subjects. Since acetylcholine inhibits hypothalamic somatostatin release, the reduced cholinergic tone in elderly subjects may result in an increased somatostatinergic tone.

Adult↗

PubMed1992

Sex-related responses of beta-endorphin, ACTH, GH and PRL to cold exposure in humans.

To establish a possible different reaction between the male and the female to short-term exposure to cold, thermal, cardiovascular and pituitary hormonal responses to cold stress were measured in eight normal men and eight women (ages 19-24). The women were eumenorrheic and were tested in the follicular phase. Each subject, lightly clad, was required to remain for 30 min in a room at an ambient temperature of 25 degrees C followed by a 30 min period in a cold room at 4 degrees C. A month later, control tests were carried out at a constant 25 degrees C temperature for 1 h in the same subjects. Skin temperature, heart rate, blood pressure and plasma levels of beta-endorphin, ACTH, cortisol, GH and PRL were measured before and after cold exposure in the two groups. Before the test, all examined parameters were similar in the two groups. During cooling, blood pressure rose and pulse rate decreased significantly in the men, but not in the women, whereas skin temperature dropped in both groups. However, after cold exposure skin temperature was significantly lower in the women than in the men. A slight, but not significant increase in beta-endorphin, ACTH, cortisol and GH levels was observed after cooling in the men, whereas the women showed significant increments of these hormones. When values of skin temperature were combined with the differential (after minus before cold test) hormonal values, significant negative correlations were found for beta-endorphin, ACTH, cortisol and GH.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1992

Inhibition by ethanol of the oxytocin response to breast stimulation in normal women and the role of endogenous opioids.

The possible inhibition exerted by ethanol on the oxytocin response to breast stimulation was tested in normal women. The possible role of endogenous opioids in the control of the oxytocin response to breast stimulation and/or ethanol action was also examined. Sixteen normal women were tested four times on the 22nd day of four consecutive regular menstrual cycles. All women underwent mechanical breast stimulation (for 10 min) with the concomitant administration of normal saline, naloxone (2 or 4 mg in an iv bolus plus 5 or 10 mg over 16 min), ethanol (50 ml in 110 ml of whisky po) or the combination of ethanol and naloxone. Plasma oxytocin levels rose about twofold after breast stimulation, with a mean peak response at 10 min. The oxytocin response to breast stimulation was not changed by the treatment with the lower (2 plus 5 mg) or the higher (4 plus 10 mg) dose of naloxone, whereas it was completely abolished by ethanol. However, when ethanol was given together with naloxone, the oxytocin rise induced by breast stimulation was only partially inhibited by ethanol (the mean oxytocin peak was 50% higher than baseline). At both doses naloxone produced similar effects. These data demonstrate that ethanol inhibits the oxytocin response to breast stimulation. Naloxone sensitive endogenous opioids do not appear to be involved in the control of the oxytocin rise induced by breast stimulation. In contrast, since naloxone partially reversed the inhibiting effects of ethanol, a partial involvement of opioid peptides in ethanol action is supposed.

Adult↗

PubMed1992

Plasma beta-endorphin, but not met-enkephalin levels are abnormal in chronic alcoholics.

Plasma beta-endorphin, met-enkephalin and ACTH concentrations were measured in 20 male alcoholics (age: 32-60 yr; duration of ethanol addiction: 13.2 +/- 6.2 yr; mean +/- SE) immediately after admission to the hospital (at a time not exceeding 8 hr from the last ethanol consumption) and after 5 weeks of forced abstinence. The results were compared with those obtained in 12 age-matched normal controls. Plasma ACTH and met-enkephalin levels were normal in alcoholics on both occasions. In contrast, in samples taken at admission to the hospital, the circulating concentrations of beta-endorphin in alcoholics were half (17.1 +/- 5.3 pg/ml; mean +/- SE) of those observed in the normal controls (34.1 +/- 6.0). beta-endorphin levels rose significantly after 5 weeks of abstinence (30.1 +/- 4.9); at this time, they were not significantly different from those observed in normal controls. These data indicate that acute alcohol consumption induces significant alterations in plasma beta-endorphin, but not met-enkephalin levels, which are reversed after 5 weeks of abstinence.

Adrenocorticotropic Hormone↗

PubMed1992

TRH test in alcoholics: relationship of the endocrine results with neuroradiological and neuropsychological findings.

Neuroradiological, neuropsychological and neuroendocrine parameters were evaluated in 20 non-depressed alcoholic men after 4 weeks (N = 11) or after at least 1 year (N = 9) of abstinence from alcohol and in normal men (N = 9). With regard to normal controls, 4-week abstinent alcoholics showed larger lateral and third ventricles, without modification in the number of cerebral sulci, and altered scores of tests evaluating subcortical and frontal function. Furthermore, in these patients the TSH (thyroid stimulating hormone) and PRL (prolactin) responses to thyrotropin releasing hormone were higher than in controls, suggesting a reduced hypothalamic control of TSH and PRL secretion. Taken together, these findings suggest the presence of a frontal-subcortical disorder in alcoholics. Patients who had been abstinent from alcohol for at least 1 year were not distinguishable from controls for neuroradiological, neuropsychological and neuroendocrine findings, suggesting that the alcohol-related brain alterations are reversible after a long period of abstinence.

Adult↗

PubMed1991

Endogenous opioid mediation of somatostatin inhibition of arginine vasopressin release evoked by insulin-induced hypoglycemia in man.

In order to establish whether endogenous opioids play a role in the control of arginine vasopressin (AVP) response to insulin-induced hypoglycemia by interacting with somatostatin (SRIH), seven normal men were submitted to an insulin (0.15 U/kg) tolerance test (ITT) in the presence or absence of naloxone (10 mg in an i.v. bolus), SRIH (4.1 micrograms/min x 90 min) or the combination of the two substances. Plasma AVP concentrations rose significantly during ITT. The AVP response remained unchanged in the presence of naloxone, whereas it was significantly reduced by the treatment with SRIH. When both SRIH and naloxone were given, the hypoglycemia induced AVP rise was similar to that observed in the control test. These results indicate the involvement of naloxone sensitive endogenous opioids in the mechanism underlying SRIH inhibitory action, but not in the mediation of the AVP response to hypoglycemia.

Adult↗

PubMed1991

Reduced ACTH/cortisol responses to naloxone in men with Parkinson's disease.

In order to establish whether the inhibitory control exerted by endogenous opioid peptides on ACTH/cortisol secretion changes in patients affected by Parkinson's disease, ten parkinsonian male subjects and eight age matched normal controls were tested with naloxone (4 mg an i.v. bolus plus 10 mg infused in two hours). In a different occasion all subjects were tested with normal saline. Experiments started at 09.00 h. Plasma ACTH and cortisol concentrations showed a slight physiological decline during saline test in both groups. In the normal controls and in the parkinsonian patients both ACTH and cortisol levels were significantly higher after naloxone administration than during saline test. However, both naloxone induced ACTH and cortisol responses were significantly higher in normal than in parkinsonian subjects. In agreement with the well-known opioid deficiency characterizing the parkinsonian brain, these data show a reduced opioid inhibitory control of ACTH/cortisol secretion in patients with Parkinson's disease.

Adrenocorticotropic Hormone↗

PubMed1991

Effect of estrogen or insulin-induced hypoglycemia on plasma oxytocin levels in bulimia and anorexia nervosa.

Plasma oxytocin (OT) levels were measured before and after stimulation with estrogens (1 mg ethynylestradiol orally) or with insulin (0.15 IU/kg)-induced hypoglycemia in seven underweight women with anorexia nervosa, eight normal weight bulimic women, and nine normal controls. Anorectic patients were amenorrhoic; they were tested at their first hospitalization (first tests) and again 8 to 9 weeks later (second tests) when they were eating normally, but were still at a low weight. In addition, anorectic women were tested 16 to 17 weeks after the first test (third tests), when their weight was restored to normal. Normal and bulimic women were tested on the fourth days of normal menstrual cycles. Insulin induced similar hypoglycemic responses in all groups. At each time point of the estrogen tests, plasma estrogen levels were similar in bulimic and normal women, whereas they were significantly lower in anorectic subjects. There were no differences in the basal levels of OT among groups. Both insulin-induced hypoglycemia and estrogen treatment produced striking OT increments in bulimic and control women, without significant differences between groups. During the first tests, no significant increase in plasma OT levels was observed in underweight anorectic women in response to both releasing stimuli. After partial weight recovery, the anorectic women showed a slight, but significant, increase in the OT responses to both insulin-induced hypoglycemia and estrogen administration. Both hypoglycemia- and estrogen-induced OT increases observed during the second tests were significantly lower in underweight anorectic patients than in normal controls. Anorectic subjects regained normal OT responsiveness to both stimuli after complete weight recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

Anorexia Nervosa↗

PubMed1991

Reduction of GH response to the GABA-B agonist baclofen in patients with major depression.

In order to establish whether alterations in the GABAergic control of GH secretion occur in male patients with major depression, the GH response to the GABAergic-B agonist baclofen (10 mg PO at 0830h) or to placebo was tested in 9 depressed men and in 10 age- and weight-matched male normal controls. The basal concentrations of GH were significantly lower in the depressed patients (0.87 +/- 0.69 ng/ml) than in the normal controls (1.57 +/- 0.33 ng/ml) (p = 0.011) and were not modified by the administration of placebo. The administration of baclofen induced a striking, significant increase in GH concentrations in the normal controls (mean peak at 90 min = 6.4 +/- 1.5 ng/ml). In contrast, a slight, nonsignificant GH increase occurred in the depressed patients after baclofen (mean peak at 90 min = 1.57 +/- 1.45 ng/ml). The GH response was significantly lower in the depressed than in the control subjects (p less than 0.001). These data indicate the presence of reduced GABAergic control of GH secretion in male depressed patients.

Adult↗

PubMed1991

Luteinizing hormone responses to gonadotropin-releasing hormone and naloxone in menstruating women with type I diabetes of different duration.

Luteinizing hormone (LH) responses to gonadotropin-releasing hormone (GnRH) (100 micrograms injected intravenously (IV)) or naloxone (4 mg injected plus 8 mg infused in 2 hours IV) were evaluated in 29 women with insulin-dependent diabetes mellitus (IDDM) (duration, group I (n = 15): less than 10 years, range 3 to 9 years; group II (n = 14): greater than 10 years, range 11 to 20 years) and in 15 normal controls, on the 22nd days of normal menstrual cycles. Both GnRH- and naloxone-induced LH responses were similar in group I diabetics and normal controls, whereas they were significantly lower in group II than in group I diabetics or normal controls. Positive correlations were found between LH responses to GnRH and naloxone, whereas negative correlations were observed between maximal LH peaks in response to GnRH or naloxone and duration of diabetes. These data indicate that a hypothalamic pituitary disorder affects LH secretion with time after the onset of IDDM.

Adult↗

PubMed1991

Reduction of baclofen-, but not sodium valproate-induced growth hormone release in type I diabetic men.

The effects of sodium valproate (a drug enhancing endogenous gamma aminobutyric acid (GABA)-ergic activity) and of the GABA analog baclofen (a GABA B receptor agonist) on serum GH levels was tested in 8 type I diabetic men and 8 normal controls. Sodium valproate (800 mg) or baclofen (10 mg) were given by mouth at 08.30 h on the experimental day. Control tests with a placebo were performed on different occasions. Basal GH levels were similar in controls and diabetic patients. Sodium valproate induced a 7 fold increase in serum GH concentrations in both groups. In contrast, baclofen-induced GH rise was significantly higher in normal controls (mean peak was 3.4 times higher than baseline) than in diabetic patients (mean peak was only 2.1 times higher than basal value). Serum GH levels did not change after placebo administration in any groups. These data suggest the presence of diabetes-induced alterations of a GABAergic pathway mediated by B receptors in the control of GH secretion. Alternatively, the data might indicate a change in diabetic men of other baclofen-sensitive neurotransmissions, different from GABA.

Adult↗

PubMed1991

Abnormal arginine vasopressin response to cigarette smoking and metoclopramide (but not to insulin-induced hypoglycemia) in elderly subjects.

Aging is known to reduce arginine vasopressin (AVP) response to volumetric stimulations and to increase AVP responses to osmotic stimuli and to administration of metoclopramide (MCP). In order to gain a better insight into the effect of age on AVP secretion, we evaluated AVP responses to cigarette smoking, MCP, and insulin-induced hypoglycemia in 30 male subjects aged 22-81 and divided into 3 groups by age. Basal AVP concentrations were similar in all groups. The AVP response during the insulin tolerance test had a similar pattern and magnitude (2.5-fold increase) in all groups. AVP responses to MCP and cigarette smoking were similar in the two younger groups, with plasma AVP levels increased 2 times by MCP and 2.5 times by cigarette smoking. In contrast, both MCP- and cigarette smoking-induced AVP rises were significantly higher in the oldest group, where plasma AVP concentrations increased 2.5 times after MCP and 3.25 times after smoking. When data of the MCP and cigarette smoking tests were combined, regression analyses showed a significant positive correlation between AVP peak responses to MCP and cigarette smoking in the oldest subjects. These data show that elderly humans have increased AVP responses not only to MCP but also to cigarette smoking, suggesting a common disorder for both alterations. In contrast, the lack of age-related changes in AVP response during the insulin tolerance test demonstrates that the mechanism underlying the AVP response to hypoglycemia is not affected by aging.

Adult↗

PubMed1991

Restoration of normal growth hormone responsiveness to GHRH in normal aged men by infusion of low amounts of theophylline.

In order to establish whether the age-related reduced growth hormone (GH) responsiveness to GH-releasing hormone (GHRH) could be improved by treatment with low amounts of theophylline, a drug mainly acting through cyclic adenosine 3', 5'-monophosphate (cAMP), and calcium-mediated mechanisms, eight adult subjects (aged 20-37) and eight elderly men (aged 64-79) were tested with GHRH (50 micrograms in an iv bolus), theophylline (1.67 mg/min for 3 h), or the combination of both drugs. The GH response to GHRH was significantly lower in the older than in the younger group (mean peaks were 4.5 and 7.5 times higher than baseline, respectively). Theophylline did not change basal GH levels in any subjects and GHRH-induced GH rise in the younger group, whereas it restored normal GH responses to GHRH in the older subjects (mean peak responses were eight times higher than baseline in both groups). These data show that in elderly subjects the mechanism underlying the GHRH-induced GH secretion may be fully activated by GHRH during treatment with low amounts of theophylline.

Adult↗