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Biomedical subjects

L De Marinis

Publications and source records attributed to L De Marinis.

At least 37 records · Page 2Linked to original sources
PubMed2000

Role of food intake in the modulation of hexarelin-induced growth hormone release in normal human subjects.

Hexarelin (HEX) is a new synthetic analog of the Growth Hormone releasing peptides and is stronger than GHRH in releasing GH in vivo. No information is available on the effect of food ingestion on HEX-induced GH secretion. On the other hand, we have previously demonstrated that food intake at lunchtime in normal subjects has an inhibitory effect on the GH response to GHRH. The aim of the present study was to investigate the effect of food ingestion on GH secretion induced by HEX as compared to GHRH in six normal men (aged 23-29 years) and six normal women (aged 24-29 years). The body weights for all subjects were within 120% of their ideal body weight, according to their sex and age. Our data confirm that HEX is much more powerful than GHRH in inducing GH release in humans, both in the fasting state (GH-AUC: 3010 +/- 695 after HEX, vs. 1339 +/- 281 after GHRH, microg/L/120 min; p<0.06) and after a meal (GH-AUC: 1523 +/- 121, after HEX, vs. 309 +/- 61, after GHRH, microg/L/120 min; p<0.06). Moreover, our study shows that food intake partially blunts the fasting GH response to HEX (GH-AUC: 3010 +/- 695 after HEX, in fasting state, vs. 1523 +/- 121 after HEX, after meal, microg/L/120 min; p<0.06; mean inhibition of AUC 41.02 +/- 7.96%), whereas it nearly abolishes the GH response to GHRH in the same subjects (GH-AUC: 1339 +/- 281 after GHRH, in fasting state, vs. 309 +/- 61 after GHRH, after meal, microg/L/120 min; p<0.06; mean inhibition of AUC 70.31 +/- 6.22%). In conclusion, our study confirms that HEX acts differently from GHRH; the GH releasing effect of HEX could be only partially influenced by the physiological metabolic or neuroendocrine food-related modifications.

Adult↗
PubMed2000

Inhibitory action on GHRH-induced GH secretion of chronic tamoxifen treatment in breast cancer.

OBJECTIVE: Previous in vitro and in vivo studies on animal models have demonstrated that tamoxifen (TAM) inhibits GH secretion. Studies in humans are conflicting. The aim of this study was to evaluate the effect of chronic TAM treatment on GH secretory dynamics in the presence of negligible endogenous oestrogens, in postmenopausal women with breast cancer. PATIENTS: Ten female patients were studied over a 6-12-month period after surgical therapy, before medical therapy, and during chronic treatment with TAM (20 mg/day p.o.). MEASUREMENTS: In all subjects we performed a standard GHRH-test (50 mg i.v. as a bolus) and compared the single time points, the peak response and the areas under the curves (AUC), before and during treatment. In basal samples, we evaluated the circulating levels of IGF-1, IGF-BP3 and their ratio, SHBG, FSH, LH, Oestradiol (E2) and PRL. GH was assayed by Immunoradiometric assay (IRMA). Insulin-like growth factor type I (IGF-I), Insulin-like growth factor-binding protein-3 (IGF-BP3), FSH, LH and PRL were measured by Radioimmunoassay (RIA). SHBG was measured by a noncompetitive liquid phase immunoradiometric assay, while E2 was measured directly in plasma by a liquid phase technique. RESULTS: TAM chronic treatment significantly reduced GH response to GHRH at single time point evaluations, GH peak response (mean decrease: 59.8 +/- 7.3%) and GH-AUC (mean decrease 53.8 +/- 8.9%). TAM also significantly reduced plasma IGF-1 levels. No significant variations were found in IGF-BP3 levels or in the IGF-1/IGF-BP3 ratio. A significant inverse correlation between SHBG and IGF-1 circulating levels was noticed during TAM treatment. CONCLUSIONS: Our data show that long-term tamoxifen treatment blocks the response of GH to exogenous GHRH and reduces IGF-1 levels, possibly by a central mechanism other than the demonstrated peripheral action. The results of this study, keeping in mind the demonstrated mitogenic role of IGF-1 in cancer proliferation, can contribute to clarify the mechanism by which TAM exerts its antiproliferative effect.

Aged↗
PubMed1999

Effect of opioid blockade on insulin and growth hormone (GH) secretion in patients with polycystic ovary syndrome: the heterogeneity of impaired GH secretion is related to both obesity and hyperinsulinism.

OBJECTIVE: To investigate the involvement of opioid tone, obesity, and hyperinsulinemia in GH secretion in women with polycystic ovary syndrome (PCOS). DESIGN: Controlled clinical study. SETTING: Catholic University of Sacred Heart School of Medicine in Rome, Italy. PATIENT(S): Twenty-two patients with PCOS and 14 healthy, normally ovulating volunteers, matched for age and body mass index. INTERVENTION(S): Patients underwent a GH-releasing hormone (GHRH) test and an oral glucose tolerance test before and after 4-5 weeks of treatment with 50 mg/d of naltrexone. MAIN OUTCOME MEASURE(S): Serum concentrations of GH, insulin, glucose, steroids, and gonadotropins, as well as the GH area under the curve (AUC-GH) and the insulin area under the curve (AUC-I), were measured before and after naltrexone treatment. RESULT(S): In patients with PCOS, the administration of naltrexone increased the GH response to the GHRH test without interfering with the insulin response to the oral glucose tolerance test. However, the GH response to the GHRH test was improved significantly only in lean patients with PCOS, whereas obese patients with PCOS did not show any improvement in GH secretion. In obese control subjects, the treatment reduced plasma basal insulin concentrations and increased the AUC-GH, whereas in lean control subjects, the treatment reduced the GHRH-induced response. In normoinsulinemic patients with PCOS, the GH response to the GHRH test increased significantly after treatment, whereas the AUC-I was not affected. In hyperinsulinemic patients with PCOS, treatment with naltrexone significantly reduced the AUC-I, whereas the AUC-GH increased only in lean hyperinsulinemic patients with PCOS. CONCLUSION(S): Naltrexone treatment improves GHRH-induced GH secretion in patients with PCOS. However, this GH response is heterogeneously represented in relation to both obesity and hyperinsulinism.

Adult↗
PubMed1999

Hypothalamic derangement in traumatized patients: growth hormone (GH) and prolactin response to thyrotrophin-releasing hormone and GH-releasing hormone.

OBJECTIVE: To study the impact of severe head injury on both basal pituitary hormone secretion and the response to exogenous synthetic hypothalamic releasing factors (TRH and GHRH) in order to evaluate sequential changes in the central control of hypophyseal secretion in the days following head injury. DESIGN: Prospective clinical study PATIENTS: 21 comatose male patients with head injuries, each intubated and ventilated, intensively monitored and having no previous endocrine problems. MEASUREMENTS: AND RESULTS The GH and PRL responses to TRH (200 microg iv), and the GH and PRL responses to GHRH (50 microg iv) were evaluated, respectively, on the days 1 and 16 and on days 2, 7and 15 after admission. Daily blood samples were also collected for GH, PRL, TSH, T3 and T4 evaluation. In the basal samples taken on days 2, 7 and 15, IGF-I and cortisol were also determined. Nitrogen balance was assessed daily. On the day 1, TRH increased GH levels from 9.8 +/- 2.2 to 22.4 +/- 6.5 mU/l but failed to induce GH release on day 16. The PRL response to TRH was normal. The GH peak response to GHRH was normal on the day 2 (35.7 +/- 13.9 mU/l), but was increased on days 7 and 15 (68.3 +/- 10.7 mU/l on day 7; 73.8 +/- 9.2 mU/l on day 15, P < 0.01 vs. day 2). We found a significant PRL response to GHRH during the whole period of observation. In the daily evaluation, nitrogen balance was negative in all patients from the day 1 to 5. On average, all patients reached a positive nitrogen balance on the day 8. Compared to the day 2, a statistical increase in IGF-I concentration was observed on days 7 and 15. CONCLUSIONS: The evaluation of pituitary dynamics in the acute phase of a severe injury demonstrates an alteration of GH and PRL secretion, which correlate with the aminergic and/or peptidergic derangements. Taken together, our data suggest augmented tone of both GHRH and somatostatin in the very acute phase, while an imbalance of releasing factors is hypothesized in the following days. The metabolic consequences of this neuroendocrine pattern could be advantageous in the rapid recovery from the cascade of events produced by the trauma, as documented by the increase in IGF-1 levels and the positive nitrogen balance.

Accidents, Traffic↗
PubMed1999

Reactive oxygen species in male infertility. Review of literature and personal observations.

Reactive oxygen species, highly reactive molecules derived from the metabolism of oxygen, play an important role in the metabolism of spermatozoa, related to the hyperactivated motility and acrosome reaction. Various studies have demonstrated that these molecules, because of their reactivity, can induce peroxidative damage on the cell, especially on the lipid membranes. The spermatozoa, owing to their structure, appear to be very sensitive to the oxidative insult. Various experimental data sustain the hypothesis that, when produced in high amounts, reactive oxygen species can induce sperm damage and become potentially responsible for some forms of unexplained infertility. The cells possess various mechanisms of defense against the oxidative insult, mainly due to antioxidant molecules. An antioxidant treatment can produce an improvement in seminal parameters and sperm function in vitro, and represents a possible form of care for selected forms of infertility.

Fertilization↗
PubMed1999

Prevalence and early diagnosis of coeliac disease in autoimmune thyroid disorders.

BACKGROUND AND AIMS: Coeliac disease is associated with several autoimmune disorders such as insulin-dependent diabetes, Sjogren's syndrome, Addison's disease and thyroid diseases. The aim of our study was to evaluate the prevalence of coeliac disease in patients affected by autoimmune thyroid diseases by means of anti-gliadin and anti-endomysial antibodies. PATIENTS: We studied 92 patients affected by autoimmune thyroid diseases (47 chronic autoimmune thyroiditis, 22 Hashimoto's thyroiditis and 23 Graves' disease). Ninety patients with non autoimmune thyroid disorders (51 multifollicular goitre, 28 solitary nodule and 11 papillary carcinoma) and 236 blood donors also took part in the study as control groups. METHODS: Total serum IgA were measured in all subjects to exclude selective IgA deficiency; then we measured anti-gliadin antibodies and anti-endomysial antibodies. In patients with anti-gliadin/anti-endomysial antibody positivity and/or with haematinic and laboratory signs of malabsorption we carried out gastrointestinal endoscopy with duodenal histological examination. RESULTS: Among the 92 patients with autoimmune thyroid disease, 4 (4.3%) showed anti-gliadin and anti-endomysial positivity and had coeliac disease; among the 90 patients with non autoimmune thyroid diseases, 1 (1.1%) had coeliac disease; finally, among the blood donors, 1 subject (0.4%) was anti-gliadin-anti-endomysium antibody positive and had coeliac disease. Those subjects presenting with only anti-gliadin antibody positivity did not have coeliac disease. CONCLUSIONS: These results show that the prevalence of coeliac disease in patients with autoimmune thyroid diseases is significantly increased when compared with the general population (p = 0.009) but not with patients affected by non autoimmune thyroid disorders (p = 0.18). We suggest a serological screening for coeliac disease in all patients with autoimmune thyroid disease measuring anti-endomysial antibodies, considering that early detection and treatment of coeliac disease are effective in preventing its complications.

Adult↗
PubMed1998

Evaluation of pre- and postprandial growth hormone (GH)-releasing hormone-induced GH response in subjects with persistent body weight normalisation after biliopancreatic diversion.

BACKGROUND: Obesity is characterised by growth hormone (GH) abnormalities, including a blunted response to stimulation and a 'paradoxical' increase after meals. The blunted GH release is reversed by a surgical intestinal bypass procedure. However, this does not mean that normal GH dynamics have been restored. The present study assessed whether post-surgical weight reduction in obese patients normalised the modulation of GH release produced by metabolic fuels. SUBJECTS: Ten obese female subjects, aged 23-54 y, were studied before and after biliopancreatic diversion (BPD). All patients, after surgery, had experienced a significant reduction in body weight (mean body mass index (BMI) 25.78 +/- 1.01 kg/m2 vs 44.68 +/- 1.73 kg/m2). Two groups were also studied as controls: Ten normal body weight female subjects and ten patients suffering from anorexia nervosa (AN, mean BMI 17.46 +/- 1.12 kg/m2). MEASUREMENTS: We have studied the GH response to a GH releasing hormone (GHRH) bolus (1 microg/kg i.v., at 13.00 h) before and after a standard meal. RESULTS: In post-BPD subjects, the GH response to GHRH in the fasting state, was clearly augmented in comparison with the pre-BPD values (peak values 18.06 +/- 4.56 vs 3.24 +/- 0.68 microg/L). In post-BPD subjects the postprandial GH response was further augmented in comparison with the fasting test (peak 30.12 +/- 4.99 microg/L, P < 0.05). This pattern was similar to that observed in anorexic patients. CONCLUSION: The surgical procedure restores a normal GH response to GHRH in the fasting state, but the 'paradoxical' GH response after meals remains present, suggesting a persistent GH derangement in such patients, which is not related to body weight per se. The surgical procedure makes obese patients similar to anorexics, in the relationships between metabolic fuels and GH secretion. The persistence of the GH postprandial response to GHRH in post-BPD subjects suggests a role for metabolic fuels in the regulation of somatostatin (SRIF) secretion.

Adult↗
PubMed1998

Provocative hypothalamopituitary axis tests in severe head injury: correlations with severity and prognosis.

OBJECTIVE: To evaluate the effect of severe head injury on both the secretion of basal pituitary hormones and the response to exogenous synthetic hypothalamic releasing factors administration. DESIGN: Prospective, clinical study. SETTING: General intensive care unit in a university teaching hospital, Italy. PATIENTS: Comatose, head-injured patients (n = 22), all intubated and mechanically ventilated, invasively monitored without previous endocrinologic problems and substitutive therapies. INTERVENTIONS: Routine neuroemergency procedures; administration of exogenous, synthetic hypothalamic releasing hormones. MEASUREMENTS AND MAIN RESULTS: Determinations of basal concentrations of growth hormone (GH), prolactin (PRL), thyroid-stimulating hormone (TSH), triiodothyronine, and thyroxine were performed daily in the first week and on days 15 and 16 after the trauma. Plasma insulin-like growth factor-I and cortisol were also determined on days 2, 7, and 15. We carried out a thyrotropin-releasing hormone (TRH) test for the evaluation of the PRL, TSH, and GH responses on days 1 and 16 after the trauma and a growth hormone-releasing hormone (GHRH) test for the evaluation of GH and PRL responses on days 2, 7, and 15 after the trauma. Outcome was evaluated at 6 mos with the GOS. Triiodothyronine showed low values, even if in the normal range; thyroxine remained in the normal range. Significant increases in insulin-like growth factor-I concentrations were observed on both days 7 and 15 compared with day 2 (p = .024 and p = .034, respectively). The GH response to GHRH was significantly greater on days 7 and 15 than in the very acute phase (p< .01 comparing days 7 and 15 vs. day 2). We found a higher GH response to GHRH on day 7 in group 1 vs. group 2 (as both peak and area under the curve, p = .018 and p = .015, respectively). No difference in GH response was detected on days 2 and 15. A "paradoxical" response of GH to TRH was observed on the day after the head trauma (basal vs. peak, p = .002) but not on day 16. The GH peak response to TRH was greater on day 1 in those patients with an unfavorable course (group 1 vs. group 2, p < .05). The TSH response to TRH was not significantly correlated to the severity of trauma, but it was significantly (p < .04) higher in group 1 than in group 2. Finally, a "paradoxical" PRL response to GHRH administration was present on day 2 (basal vs. peak, p=.0003), day 7 (basal vs. peak, p = .01), and on day 15 after the trauma (basal vs. peak, p = .04). CONCLUSIONS: Some of the responses to provocative tests have been identified as "paradoxical" and seem to have a great importance in the definition of prognosis in severe head-injured patients, specifically the GH response to TRH and the PRL response to GHRH that are significantly correlated with outcome.

Adolescent↗
PubMed1997

Physiological role of the opioid-cholinergic interaction in growth hormone neuroregulation: effect of sex and food intake.

Studies performed in animals and humans have suggested a functional interaction between opioid and cholinergic systems in the control of growth hormone (GH) secretion. Moreover, the sex-dependent modulation of GH secretion in humans is well established. To investigate the role of sex and food intake in the regulation of the reciprocal influences of opioids and acetylcholine in the modulation of GH secretion, we studied the GH response to pyridostigmine (PYR) alone and during a naloxone (NAL) infusion in a group of normal men and women before a meal (at 1:00 PM) and postprandially. In women, the response of GH to PYR alone before the meal was significantly lower than in the men (area under the curve [AUC], mean +/- SEM, 320.18 +/- 87.16 v 1,031.06 +/- 333.21 micrograms/L/90 min, P < .01). Before the meal, NAL completely abolished the response of GH to PYR in men (AUC, 1,031.06 +/- 333.21 v 16.50 +/- 7.50 micrograms/L/90 min, P < .01), whereas infusion of NAL did not significantly modify the GH response to PYR in women. Consumption of the meal significantly decreased PYR-induced GH release in both women (AUC, 21.75 +/- 12.75 v 320.18 +/- 87.16 micrograms/L/90 min, P < .05) and men (AUC, 45.75 +/- 18.75 v 1,031.06 +/- 333.21 micrograms/L/90 min, P < .01). Conversely, food intake did not change the effects of NAL infusion on the GH response to PYR either in women or in men. We conclude that the sex-dependent opioid modulation of PYR-induced GH secretion is observed before a meal but not in the postprandial state. Food intake may be hypothesized to influence the cholinergic regulation of GH secretion and the sex-dependent opioid modulation of central cholinergic tone.

Adult↗
PubMed1997

Impact of long-term naltrexone treatment on growth hormone and insulin secretion in hyperandrogenic and normal obese patients.

The growth hormone (GH) response to stimulation tests is impaired in obesity. Moreover, obese patients exhibit a "paradoxical" increase of GH to GH-releasing hormone (GHRH) stimulation after food ingestion; this paradoxical response is reversed by naloxone infusion. On the other hand, beta-endorphin seems to exert profound effects on insulin release. Recent studies also demonstrated an impairment of GH response to several stimuli in polycystic ovary syndrome (PCOS), a condition associated with obesity, hyperinsulinism, and insulin resistance. Chronic inhibition of opioid tone by the opioid antagonist naltrexone (NTX) is able to reduce the insulin response to an oral glucose tolerance test (OGTT) in hyperinsulinemic PCOS patients. Since insulin and GH may reciprocally influence their secretion and the opioid system may have a role in the pathogenesis of hyperinsulinemia and reduced GH secretion, we have explored the involvement of these neuroendocrine mechanisms in essential obesity and in obesity associated with hyperandrogenism by a long-term treatment with an opiate antagonist. We tested seven obese patients affected by PCOS, seven matched women with essential obesity (EO), and five non-obese control subjects. All patients, in the follicular phase, underwent an OGTT (75 g) and basal hormone assay. Two days later, patients were subjected to a GHRH test. The patients then had 4 weeks of treatment with NTX 50 mg/d. Following continuation of the treatment, OGTT and GHRH tests were repeated. Insulin-like growth factor-I (IGF-I) and IGF-binding protein-3 (IGFBP-3) plasma concentrations were also determined in the basal condition before and after NTX treatment. NTX treatment reduced fasting insulin levels in patients with EO (P < .05) and restored a normal GH response to GHRH without affecting IGF-1 and IGFBP-3 levels. In PCOS subjects, NTX reduced the insulin response to a glucose load and failed to modify the blunted GH response to GHRH. Our data suggest a significant difference in opioid system function in PCOS and EO subjects, indicating a particular form of obesity in PCOS. The opiate antagonist treatment in EO may act through the reduction of negative insulin feedback on GH secretion. In PCOS patients, the failure to improve GH secretion in obese hyperandrogenized patients may be related to a high opioidergic tone or to the inhibitory predominance of other neurotransmitters.

Adult↗
PubMed1997

Influence of chronic Naltrexone treatment on growth hormone and insulin secretion in obese subjects.

OBJECTIVE: Recent studies have demonstrated the restoration of a normal 24 h GH profile induced by a reduction of insulinaemia after weight loss, suggesting a reciprocal relationship between plasma insulin and GH concentrations. We aimed to clarify if an opiate-induced reduction in plasma insulin could affect GH secretion in obesity. DESIGN: We have studied the insulin response to an oral glucose tolerance test (OGTT) and the GH response to GHRH before and after prolonged treatment with Naltrexone (NTX). C-peptide, IGF-I, IGFBP-3 plasma levels and the IGF-I/IGFBP-3 molar ratio were also determined. SUBJECTS: Twelve obese women (aged 25-41 y; Body mass index (BMI): 31-39 kg/m2) and six lean normal women (aged 25-38; BMI: 19.8-23.1 kg/m2). MEASUREMENT: GH was determined by the IRMA method; insulin, C-peptide, IGF-I and IGFBP-3 were assayed by the RIA method. For molar comparison between IGF-I and IGFBP-3 we have considered 30.5 kDa the molar weight of IGFBP-3. Results are expressed as mean +/- s.e.m. RESULTS: We observed a significant decrease in basal concentration of both insulin (230.1 +/- 34.9 vs 133.2 +/- 16.9 pmol/L; P < 0.005) and C-peptide (3.7 +/- 0.3 vs 2.4 +/- 0.1 micrograms/L; P < 0.02). No modifications in the insulin secretory response to the OGTT were observed. A significant increase of the GHRH-induced GH peak response (7.7 +/- 1.4 vs 19.7 +/- 3.1 micrograms/L; P < 0.01) and GH-AUC (533 +/- 151 vs 1415 +/- 339 micrograms/L/120 min; P < 0.01) was found after NTX treatment. A negative correlation was found between basal insulin and GH peak values, both before (r = -0.641, P = 0.027) and after NTX (r = -0.714, P = 0.013). No modifications were found in IGF-I, IGFBP-3 and IGF-I/IGFBP-3 molar ratio. Moreover, NTX affected neither the insulin response to OGTT or IGF-I, IGFBP-3 and IGF-I/IGFBP-3 molar ratio in a group of six lean controls. Conversely, NTX significantly reduced the GH response to GHRH, when expressed as both peak and AUC values. CONCLUSIONS: The opiate antagonist significantly reduced basal insulin concentrations and augmented the GH response to GHRH in obese subjects. In the absence of modifications in IGF-I and IGFBP-3 plasma levels and their molar ratio, we propose that insulin may exert a negative feedback on GH secretion.

Adult↗
PubMed1997

Influence of chronic naltrexone treatment on growth hormone secretion in normal subjects.

OBJECTIVE: To verify if a chronic opioid blockade could affect the GH/IGF-I axis. DESIGN: We have investigated the effects of naltrexone (NTX) treatment on GH response to GHRH in normal women. METHODS: GHRH test (50 micrograms i.v.) performed in seven normal female volunteers (age 25-38 years, with a body mass index ranging from 19.8 to 23.1 kg/m2) before and after 4-weeks NTX treatment (50 mg p.o. daily). RESULTS: Basal GH, IGF-I, insulin-like growth factor binding protein-3 (IGFBP-3) plasma levels and the IGF-I/IGFBP-3 molar ratio remained unaffected by NTX. NTX significantly reduced the GH peak values (15.52 +/- 3.59 vs 4.78 +/- 0.49 micrograms/l; P < 0.01), and GH area under curve (918.93 +/- 253.96 vs 401.09 +/- 79.63 micrograms/l; P < 0.01). CONCLUSIONS: This finding suggests that the long-term opioid receptor blockade has an inhibitory role on GHRH-induced GH secretion. A central influence on neurotransmitter control of GH might be hypothesised. The inhibition of stimulated GH release, without interference with the basal level, could indicate an enhanced somatostatin secretion and/or activity. Opioids could be involved only in the regulation of GH dynamics and not in basal secretion. Nevertheless, a direct involvement of opioids at the pituitary level, which could be modified by NTX, cannot be excluded.

Adult↗
PubMed1996

Pre- and postprandial pyridostigmine and oxiracetam effects on growth hormone secretion in anorexia nervosa.

Previous studies have shown that food ingestion is not capable of inhibiting the GHRH-induced GH release in anorexia nervosa, at variance with what is observed in normal subjects. Moreover, a cholinergic alteration has been hypothesized in this disorder. In a group of 24 anorectic patients in a stabilized phase of the illness, we tested, before and after a standard meal, the GH response to GHRH alone and after pre-treatment with pyridostigmine, an inhibitor of acetylcholinesterase, and, on a different day, with oxiracetam, which stimulates the central cholinergic neurones. The GH response to GHRH was significantly increased by both drugs in a fasting state. The postprandial response was not significantly modified by pyridostigmine nor by oxiracetam. Neither of these compounds was able to enhance the postprandial GH 'paradoxical' response to GHRH in anorectic patients. The lack of effect of both groups postprandially also suggests a suppression of somatostatinergic activity.

Acetylcholinesterase↗
PubMed1996

Naloxone influence on the growth hormone, prolactin and thyrotropin response to thyrotropin releasing hormone in acromegalic patients.

In order to gain insight into the neuroendocrine mechanism underlying the paradoxical GH response to TRH in acromegalic patients, we have investigated the effect of an infusion of Naloxone (Nal, 1.6 mg/hr for two hours), on a TRH test performed both in responder (n = 9) and non-responder (n = 5) acromegalic patients. The response of GH, PRL and TSH to TRH injection were evaluated. NAL did not exert significant variations in the GH response, even if different patterns of GH response during NAL were observed in the group of TRH-responder patients. Similarly, TRH-induced PRL response was not significantly affected by the infusion of an opiate antagonist. On the contrary, a significant inhibition of the TSH response was observed in the group of TRH-responder patients (delta TSH after TRH 4.76 +/- 1.11 microU/ml, after NAL + TRH 2.81 +/- 0.99 microU/ml, p < 0.05). No significant effects were observed in the TRH non-responder patients (delta TSH after TRH 4.58 +/- 1.44 microU/ml, after NAL + TRH 6.26 +/- 3.27 microU/ml). The differences observed in the two groups of patients could be ascribed to a different endogenous somatostatinergic tone and could furnish a prognostic indication in acromegalic patients.

Acromegaly↗
PubMed1995

GH response to oral and intravenous glucose load in acromegalic patients.

The lack of inhibition of Growth Hormone (GH) levels after glucose load is considered a marker of inappropriate GH secretion in acromegaly. In order to investigate the physiopathology of this phenomenon, we have studied the GH variations after an oral glucose load (0.75 g/kg BW per os, OGTT) or intravenous glucose bolus (25 g i.v., IVGTT), in a group of 12 acromegalic patients, aged 20 +/- 69 yr (mean 48), 5 males and 7 females, with basal GH levels ranging from 11 to 76.2 ng/ml. The results indicate that only a group of acromegalic patients (group 1) had a partial GH inhibition after OGTT (mean decrease: 56.4 +/- 4.2%), but in no patients GH levels were influenced by intravenous administration of glucose. It is possible that in group 1 patients, the gastroenteric response could partially influence the GH secretion by the pituitary tumor, probably due to an increased peripheral somatostatin release. The dissociation of the GH response to OGTT and IVTT could indicate a supersensitivity to peripheral somatostatin, related to a deficiency in central somatostatinergic tone and therefore represent a more unfavourable prognostic sign.

Acromegaly↗
PubMed1994

Opioid dysregulation in anorexia nervosa: naloxone effects on preprandial and postprandial growth hormone response to growth hormone-releasing hormone.

Previously, we have shown that in the opposite extremes of nutritional status, obesity and anorexia nervosa (AN), growth hormone (GH) response to growth hormone-releasing hormone (GH-RH) is not inhibited by the ingestion of a normal 800-cal meal consumed at lunch time (1 PM), which is at variance with results in normal subjects. However, in obese patients the postprandial increase in GH response to GH-RH is inhibited by an infusion of naloxone (NAL). In this study we have tested anorectic patients, performing the following tests at 1 PM: GH-RH test (50 micrograms IV) or, in a different day session, NAL (1.6 mg/h, starting 30 minutes before GH-RH) + GH-RH test (50 micrograms IV). The tests were performed in the following three different experimental conditions: (1) short-term fasting studies (lasting from breakfast), (2) long-term fasting studies (from midnight of the day before) and (3) postprandial studies (after a standard meal consumed 1 hour before the test). In AN, the GH response to GH-RH was not influenced by NAL infusion at 1 PM, in both short- and long-term fasting studies (short-term fasting: peak values after GH-RH alone, 26.5 +/- 6.5 ng/mL, during NAL, 28.0 +/- 3.3 ng/mL; long-term fasting: peak values after GH-RH alone, 32.2 +/- 6.8 ng/mL, during NAL, 30.6 +/- 4.0 ng/mL). A partial NAL-inhibitory effect was instead observed in postprandial studies, as evidenced by the calculation of areas under the curve ([AUCs] 1,662.1 +/- 90.0 after GH-RH alone v 1,090.5 +/- 245.4 ng/mL/h during NAL).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Coenzyme Q10 levels in human seminal fluid: diagnostic and clinical implications.

The levels of Coenzyme Q10 (CoQ10) were determined by HPLC in seminal fluid samples obtained from 77 patients who performed a standard semen analysis for infertility, previous phlogosis or varicocele. CoQ10 was determined in total seminal fluid (n = 60), in seminal plasma (n = 44) and in the cell pellet (n = 37). The molecule, in total fluid, showed a linear correlation with sperm count and motility. In the pellet of spermatozoa, a trend toward an inverse correlation between CoQ10 (expressed as ng/10(6) cells) and semen parameters could be observed. A different pattern was shown in varicocele patients, in whom, in total fluid, the correlation between CoQ10 and sperm count was preserved, but the one between CoQ10 and sperm motility was lacking; moreover, a higher proportion of CoQ10 was present in seminal plasma, and the inverse trend between cellular CoQ10 and sperm count and motility was not observed. These data suggest a pathophysiological role of ubiquinone in human seminal fluid and a molecular defect in the spermatozoa of varicocele patients.

Adult↗