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GH Levels (gh + level)
Selected AbstractsGreater growth hormone and insulin response in women than in men during repeated bouts of sprint exerciseACTA PHYSIOLOGICA, Issue 2 2009M. Esbjörnsson Abstract Aim:, In a previous study, sprint training has been shown to increase muscle cross-sectional area in women but not in men [Eur J Appl Physiol Occup Physiol 74 (1996) 375]. We hypothesized that sprint exercise induces a different hormonal response in women than in men. Such a difference may contribute to explaining the observed gender difference in training response. Method:, Metabolic and hormonal response to three 30-s sprints with 20-min rest between the sprints was studied in 18 physically active men and women. Results:, Accumulation of blood lactate [interaction term gender (g) × time (t): P = 0.022], and plasma ammonia (g × t: P < 0.001) after sprint exercise was greater in men. Serum insulin increased after sprint exercise more so in women than in men (g × t: P = 0.020), while plasma glucose increased in men, but not in women (g × t: P < 0.001). Serum growth hormone (GH) increased in both women and men reaching similar peak levels, but with different time courses. In women the peak serum GH level was observed after sprint 1, whereas in men the peak was observed after sprint 3 (g × t; P < 0.001). Serum testosterone tended to decrease in men and increase in women (g × t: P = 0.065). Serum cortisol increased approx. 10,15% after sprint exercise, independent of gender (time: P = 0.005). Conclusion:, Women elicited a greater response of serum GH and insulin to sprint exercise. This may contribute to explaining the earlier observed muscle hypertrophy in women in response to sprint training. [source] Likelihood of persistent GH deficiency into late adolescence: relationship to the presence of an ectopic or normally sited posterior pituitary glandCLINICAL ENDOCRINOLOGY, Issue 2 2009P.G. Murray Summary Objectives, The presence of an ectopic posterior pituitary gland (EPP) in childhood is associated with isolated GH deficiency (IGHD) and multiple pituitary hormone deficiency. GHD in late adolescence has been defined as a peak GH level <5 ,g/l. The aim of this study was to identify the likelihood of persistent GHD in late adolescence in patients with an EPP compared with those with a normally sited posterior pituitary (NPP). Methods, In 18 patients with an EPP and 15 patients with an NPP, clinical, biochemical and radiographic data were collected. Results, In the EPP vs. the NPP group, the change in peak GH levels at the end of growth was less (+0·4[95% confidence interval (CI) - 0·8 to 2·7] vs. +4·1[95%CI + 0·4 to +10·5] ,g/l, P -value for ancova = 0·03, after adjustment for age and sex). Using a peak GH level of <5 ,g/l as a cut-off for GHD, 66% of EPP subjects compared with 40% of NPP subjects had GHD (P = 0·3). Hundred per cent of EPP subjects had a peak GH level on retesting <10 ,g/l, compared with 40% of NPP subjects (P < 0·001). Conclusion, It is important to document GH status at the end of growth, even if there is a structural abnormality of the hypothalamic,pituitary axis. The presence of an EPP compared to an NPP increases the likelihood of persistent GHD by 26%. As all EPP patients had a peak GH level of <10 ,g/l, the cut-off for persistent GHD in late adolescence may need to be revised. [source] Long-term (up to 18 years) effects on GH/IGF-1 hypersecretion and tumour size of primary somatostatin analogue (SSTa) therapy in patients with GH-secreting pituitary adenoma responsive to SSTaCLINICAL ENDOCRINOLOGY, Issue 2 2007Jean Christophe Maiza Summary Context The role of somatostatin analogues (SSTa) in the treatment of acromegaly. Objective To evaluate the antihormonal and antitumour efficacy of long-term (up to 18 years) primary treatment with SSTa in patients with GH-secreting pituitary adenoma responsive to SSTa. Design An open, prospective, single-centre, clinical study. Patients Thirty-six acromegalic patients, aged 17,75 years (postoral glucose tolerance test GH > 1 µg/l, increased IGF-1 for age and sex), were monitored in a single centre and treated with SSTa as first-line therapy. The mean pretreatment GH level was 13·5 ± 3·1 µg/l, and IGF-1 (as a percentage of the value over the normal range) was 302 ± 26%. The patients had macroadenoma (n = 25), microadenoma (n = 8) or empty sella turcica (n = 3). The mean duration of treatment was 8 years (range 3,18 years). Hormonal and morphological monitoring was undertaken after 6 months, and then the patients were followed annually. Results After 1 year, the mean GH and IGF-1 levels had reduced considerably (GH: 2·4 ± 0·3 µg/l; IGF-1; 174 ± 14%, P < 0·01), and they continued to decrease over 10 years, with a mean GH level of 1·6 ± 0·1 µg/l and IGF-1 of 123 ± 18% (P = 0·02). GH < 2 µg/l, normal IGF-1, or both were observed in 25 (70%), 24 (67%) and 21 (58%) patients, respectively. The mean reduction in tumour volume was 43% (range 13,97%) and shrinkage > 20% was obtained in 21 patients (72%). SSTa treatment was well tolerated with few digestive or metabolic side-effects. Conclusion Long-term (up to 18 years) treatment with SSTa used as first-line therapy is effective from both an antihormonal and antitumour perspective, and is well tolerated in acromegalic patients. [source] Lower levels of circulating IGF-I in Type 1 diabetic women with frequent severe hypoglycaemia during pregnancyDIABETIC MEDICINE, Issue 7 2008L. Ringholm Nielsen Abstract Aims Severe hypoglycaemia is a significant problem in pregnant women with Type 1 diabetes. We explored whether frequent severe hypoglycaemia during pregnancy in women with Type 1 diabetes is related to placental growth hormone (GH) and insulin-like growth factor I (IGF-I) levels. Methods A prospective, observational study of 107 consecutive pregnant women with Type 1 diabetes. Blood samples were drawn for IGF-I and placental GH analyses at 8, 14, 21, 27 and 33 weeks. Severe hypoglycaemic events were reported within 24 h. Results Eleven women (10%) experienced frequent severe hypoglycaemia (, 5 events), accounting for 60% of all events. Throughout pregnancy, IGF-I levels were 25% lower in these women (P < 0.005) compared with the remaining women, despite similar placental GH levels. Eighty per cent of the severe hypoglycaemic events occurred before 20 weeks when IGF-I levels were at their lowest. This finding was not explained by differences in insulin dose, median plasma glucose levels or glycated haemoglobin. History of severe hypoglycaemia the year preceding pregnancy and impaired hypoglycaemia awareness,being the only predictors of frequent severe hypoglycaemia in a logistic regression analysis,were not associated with IGF-I or placental GH levels at 8 weeks. Conclusions In women with Type 1 diabetes experiencing frequent severe hypoglycaemia during pregnancy, IGF-I levels are significantly lower compared with the remaining women despite similar placental GH levels. IGF-I levels are lowest in early pregnancy where the incidence of severe hypoglycaemia is highest. IGF-I may be a novel factor of interest in the investigation of severe hypoglycaemia in patients with Type 1 diabetes. [source] Influence of plasma lipid changes in response to 17,-oestradiol stimulation on plasma growth hormone, somatostatin, and thyroid hormone levels in immature rainbow troutJOURNAL OF FISH BIOLOGY, Issue 3 2001F. Mercure Plasma total lipids were significantly higher in 17,-oestradiol(E2)-treated immature rainbow trout Oncorhynchus mykiss at week 4 after implantation, due to increases in polar and neutral lipids. The lipid classes responding were phosphatidylcholine, phosphatidylinositol, phosphatidylethanolamine, sterols and sterol esters, in a proportion that approximately reflected the increase in plasma vitellogenin (VtG) levels as measured by a non-competitive enzyme-linked immunosorbent assay (ELISA). Plasma non-esterified fatty acids and triacylglycerol were not affected by E2 treatment. Plasma growth hormone GH levels were increased, and plasma somatostatin-14 (SRIF) levels decreased in E2 -treated fish, responses which could be secondary to elevated plasma lipid (VtG) content, although a direct E2 action on somatotroph function is possible. Plasma T4 concentrations were not affected by E2 treatment, but plasma T3 concentrations were significantly lower than in controls 1 week after implantation when plasma E2 concentrations were the highest; this is in support of the hypothesis that E2 has a suppressive action on T3 production. [source] Effect of propranolol plus exercise on melatonin and growth hormone levels in children with growth delayJOURNAL OF PINEAL RESEARCH, Issue 2 2001A. Muñoz-Hoyos The pineal gland in humans is under both ,- and ,-adrenergic control, although it seems that ,1 -adrenoceptors are mainly implicated in melatonin secretion. In the present study, we evaluated the role of ,-adrenergic innervation on melatonin production and its relation with the production of growth hormone (GH). Thirty-four children (15 males and 19 females, mean age 10.5±0.8 years) from the University of Granada Hospital were studied. The children were included in a protocol for the evaluation of growth delay using the propranolol+exercise test. This standardized test allowed us to study simultaneously the role of an unspecific ,-adrenergic blocker such as propranolol and of an adrenergic stimulus such as exercise on the pineal production of melatonin. Changes in plasma levels of melatonin and GH were determined at basal, 120 and 140 min after the test was applied. Hormonal determinations were carried out by commercial radioimmunoassay kits previously standardized in our laboratory. The results show a significant decrease in plasma melatonin levels at 120 and 140 min after the test (P<0.05), whereas GH levels increased significantly at 140 min (P<0.001). The decrease of melatonin levels was a consequence of the test, since in a control group, the circadian decay of melatonin was significantly less pronounced (P<0.05). These data suggest an inverse relationship between melatonin and GH after the propranolol+exercise test, and the reduction in melatonin may be related to its depletion by exercise-induced oxidative stress. [source] Secretion of Prolactin and Growth Hormone in Relation to Ovarian Activity in the DogREPRODUCTION IN DOMESTIC ANIMALS, Issue 3-4 2001HS Kooistra In pregnant bitches an apparent increase in plasma prolactin concentrations is observed during the second half of pregnancy, mean plasma prolactin concentrations peak on the day of parturition, fall for the next 24,48 h and then rise again. During lactation, high plasma prolactin concentrations are observed. Plasma prolactin levels in non-pregnant bitches appear to be lower than in pregnant animals, particularly in the last part of the luteal phase. Pulsatile secretion of prolactin has been observed during the luteal phase and mid-anoestrus. Progression of the luteal phase is found to be associated with an increase in prolactin release. The association of a strong increase of prolactin release and a decrease of plasma progesterone concentrations has also been demonstrated in overtly pseudopregnant bitches. Elevated prolactin secretion during progression of the luteal phase in the bitch may play a role in mammogenesis and is important because of the luteotrophic action of prolactin. Acromegaly is a syndrome of tissue overgrowth and insulin resistance due to excessive growth hormone (GH) production. In the bitch, acromegaly can be induced either by endogenous progesterone or by exogenous progestagens. Progestagen-induced GH production in this species originates from foci of hyperplastic ductular epithelium of the mammary gland. Pulsatile secretion of GH has been observed in normal cyclic bitches. In contrast with the pulsatile GH secretion seen in healthy dogs, the progestagen-induced plasma GH levels in bitches with acromegaly do not have a pulsatile secretion pattern. Just as with prolactin, the plasma progesterone levels influence the secretion pattern of GH in the bitch. The pulsatile secretion pattern of GH changes during the progression of the luteal phase in healthy cyclic bitches, with higher basal GH secretion and less GH being secreted in pulses during the first part of the luteal phase. The progesterone-induced GH production may promote the proliferation and differentiation of mammary gland tissue during the luteal phase of the bitch by local autocrine/paracrine effects and may exert endocrine effects. [source] Likelihood of persistent GH deficiency into late adolescence: relationship to the presence of an ectopic or normally sited posterior pituitary glandCLINICAL ENDOCRINOLOGY, Issue 2 2009P.G. Murray Summary Objectives, The presence of an ectopic posterior pituitary gland (EPP) in childhood is associated with isolated GH deficiency (IGHD) and multiple pituitary hormone deficiency. GHD in late adolescence has been defined as a peak GH level <5 ,g/l. The aim of this study was to identify the likelihood of persistent GHD in late adolescence in patients with an EPP compared with those with a normally sited posterior pituitary (NPP). Methods, In 18 patients with an EPP and 15 patients with an NPP, clinical, biochemical and radiographic data were collected. Results, In the EPP vs. the NPP group, the change in peak GH levels at the end of growth was less (+0·4[95% confidence interval (CI) - 0·8 to 2·7] vs. +4·1[95%CI + 0·4 to +10·5] ,g/l, P -value for ancova = 0·03, after adjustment for age and sex). Using a peak GH level of <5 ,g/l as a cut-off for GHD, 66% of EPP subjects compared with 40% of NPP subjects had GHD (P = 0·3). Hundred per cent of EPP subjects had a peak GH level on retesting <10 ,g/l, compared with 40% of NPP subjects (P < 0·001). Conclusion, It is important to document GH status at the end of growth, even if there is a structural abnormality of the hypothalamic,pituitary axis. The presence of an EPP compared to an NPP increases the likelihood of persistent GHD by 26%. As all EPP patients had a peak GH level of <10 ,g/l, the cut-off for persistent GHD in late adolescence may need to be revised. [source] Control of IGF-I levels with titrated dosing of lanreotide Autogel over 48 weeks in patients with acromegalyCLINICAL ENDOCRINOLOGY, Issue 2 2008Philippe Chanson Summary Background, An essential criterion for control of acromegaly is normalization of IGF-I levels. Somatostatin analogues act to suppress IGF-I and GH levels. Objective, To assess the efficacy and safety of 48 weeks titrated dosing of lanreotide Autogel. Design, Open-label, multicentre, phase III, 48-week trial. Methods, Patients with active acromegaly (IGF-I levels > 1·3 times upper limit of age-adjusted normal range) were recruited. Twelve injections of lanreotide Autogel were given at 28-day intervals: during the 16-week fixed-dose phase, patients received 90 mg; in the 32-week dose-titration phase, patients received 60, 90 or 120 mg according to GH and IGF-I levels. Intention-to-treat analysis was performed to determine the proportion of patients with normalized age-adjusted IGF-I levels at study end. Secondary evaluations included GH levels, clinical acromegaly signs and safety. Results, Fifty-seven of 63 patients completed the study. Lanreotide Autogel resulted in normalized age-adjusted IGF-I levels in 27 patients (43%, 95% CI 31,55). Mean GH levels decreased from 6·2 to 1·5 µg/l at study end, with 53 of 62 patients (85%) having GH levels , 2·5 µg/l (95% CI 76·7,94·3) and 28 of 62 patients (45%) with levels < 1 µg/l (95% CI 32·8,57·6). Twenty-four (38%) had both normal IGF-I levels and GH levels , 2·5 µg/l. Acromegaly symptoms reduced significantly in most patients throughout the study. The most common adverse events were gastrointestinal, as expected for somatostatin analogues. Conclusions, Using IGF-I as primary end-point, 48 weeks lanreotide Autogel treatment, titrated for optimal hormonal control, controlled IGF-I and GH levels effectively, reduced acromegaly symptoms and was well tolerated. [source] Surgical debulking of pituitary macroadenomas causing acromegaly improves control by lanreotideCLINICAL ENDOCRINOLOGY, Issue 6 2008N. Karavitaki Summary Background, Macroadenomas causing acromegaly are cured surgically in only around 50% of patients. Primary medical treatment with somatostatin analogues has been suggested to be a means of treating patients with a potentially poor surgical outcome. Previous retrospective studies have also suggested that surgical debulking of pituitary tumours causing acromegaly improves control by somatostatin analogues. No prospective study using lanreotide has been carried out thus far to assess whether this is the case. Objective, We carried out a prospective study to assess whether surgical debulking of pituitary macroadenomas causing acromegaly improved the subsequent control of acromegaly by the somatostatin analogue lanreotide. Patients and methods, We treated 26 consecutive patients [10 males and 16 females , median age 53·5 years (range 22,70)] with macroadenoma causing acromegaly unselected for somatostatin response for 16 weeks with lanreotide, maximizing GH and IGF-I suppression, if necessary, by incremental dosing. Surgical resection was carried out and the patients were re-assessed off medical treatment at 16 weeks following surgery. Those with nadir GH > 2 mU/l in the oral glucose tolerance test (OGTT) and a mean GH in the GH day curve (GHDC) > 5 mU/l were subsequently restarted on lanreotide and the responses were assessed at the same time points as during the preoperative lanreotide treatment. Results, GH values fell on lanreotide treatment and prior to surgery they were considered ,safe' (mean GH in GHDC < 5 mU/l) in eight patients (30·7%). After surgery, they were ,safe' in 18 patients (69·2%). The figures for normal IGF-I were 11 (42·3%) before surgery and 23 (88·5%) after surgery. After surgery, six patients had nadir GH > 2 mU/l in the OGTT and ,unsafe' GH levels (mean GH in GHDC > 5 mU/l); on re-exposure to lanreotide, GH levels fell in all patients and at the end of 16 weeks postsurgery, they were ,safe' in three of them (50%) (P < 0·05). Pituitary tumour volume was also assessed prospectively, preoperatively on lanreotide and showed a mean fall of 33·1%. Eighty-three percent of patients had > 20% shrinkage. Conclusions, In this first prospective study using lanreotide, surgical debulking of pituitary tumours causing acromegaly improved subsequent postoperative control by the somatostatin analogue lanreotide. Surgery should, therefore, be considered in patients with macroadenoma causing acromegaly, even if there is little prospect of surgical cure. Lanreotide causes significant pituitary tumour shrinkage in the majority of patients. [source] Perioperative plasma active and total ghrelin levels are reduced in acromegaly when compared with in nonfunctioning pituitary tumours even after normalization of serum GHCLINICAL ENDOCRINOLOGY, Issue 1 2007Takakazu Kawamata Summary Objective, Ghrelin is a novel gastric peptide known to stimulate GH secretion, but the relationship between ghrelin and the GH-insulin-like growth factor (IGF)-1 axis in GH excess or deficiency is poorly understood. This study investigated dysregulation of ghrelin secretion in acromegaly and its short-term postoperative recovery. Methods, A prospective study was conducted on eight patients who underwent complete transsphenoidal resection of GH-producing pituitary adenomas (acromegaly group) and 22 for endocrinologically nonfunctioning pituitary tumours (control group). Active and total plasma ghrelin levels were measured serially before and after surgery. Results, Preoperative active and total plasma ghrelin concentrations (mean ± SD; fmol/ml) were significantly reduced in acromegalic patients when compared with those in the controls (9·6 ± 4·3 and 157·4 ± 65·6 vs. 21·8 ± 13·0 and 267·1 ± 111·4; P = 0·023 and P = 0·021, respectively). Both levels were still significantly suppressed on postoperative Day 7 in the acromegaly group when compared with those in the control group (11·7 ± 4·3 and 197·8 ± 68·9 vs. 22·5 ± 12·6 and 302·7 ± 100·0; P = 0·038 and P = 0·018, respectively). The ratios of active to total ghrelin were not significantly different between the two groups before and after operation. In acromegalic patients, active and total ghrelin levels remained significantly suppressed even after normalization of serum GH levels. Conclusions, The putative negative feedback mechanism of GH on ghrelin secretion may in part account for the low ghrelin levels observed in acromegalic patients, and the mechanism may persist even after normalization of serum GH. [source] Serum ghrelin concentrations in patients with chronic renal failure undergoing dialysisCLINICAL ENDOCRINOLOGY, Issue 1 2006Pedro Iglesias Summary Background, ,Ghrelin is a recently discovered protein hormone mainly synthesized in the gastric endocrine cells. This hormone not only is a potent growth hormone secretagogue but also is involved in the regulation of food ingestion and energy metabolism. Derangements in ghrelin secretion in patients with chronic renal failure (CRF) have not been fully evaluated. Objective, ,Our aim has been to quantify serum concentrations of total ghrelin in a group of patients with CRF on chronic therapy with both haemodialysis (HD) and peritoneal dialysis (PD) in comparison with a group of patients on conservative management (predialysis). Patients and measurements, ,We studied 68 CRF patients treated by HD (n = 30, 16 men, age 61·2 ± 1·8 years) and PD groups (n = 38, 21 men, age 54·4 ± 1·7 years). A group of 19 uraemic patients on conservative management served as the control. Serum concentrations of ghrelin, leptin, insulin, IGF I and GH were measured in all subjects. Results, ,Patients undergoing HD showed similar concentrations of ghrelin in comparison with the control group (9491 ± 787 vs 9280 ± 918 pg/ml, NS). However, PD patients exhibited baseline ghrelin concentrations significantly lower than those found in patients on conservative management (3230 ± 216 pg/ml, P < 0·0001). Men and women showed similar serum ghrelin levels in both HD (9845·9 ± 1071 vs 9085 ± 1194 pg/ml) and PD patients (3214 ± 297 vs 3250 ± 324 pg/ml). Hypertension and diabetes mellitus did not influence ghrelin levels. Serum GH levels were positively correlated with serum ghrelin concentrations in both HD (r = 0·46, P < 0·05) and PD (r = 0·53, P < 0·001) patients; however, no relationships between ghrelin, leptin, insulin and IGF I were found. Conclusions, ,These results suggest that PD is accompanied by a striking decrement in baseline ghrelin concentrations in comparison with values found both in HD and control patients. Further studies are necessary to determine mechanisms involved in ghrelin regulation in uraemic patients. [source] | |||||||||||||