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GH Response (gh + response)

Distribution by Scientific Domains
Medical Sciences100%

Kinds of GH Response

  • peak gh response
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    Selected Abstracts

    Growth hormone and changes in energy balance in growth hormone deficient adults

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 9 2008
    D. Deepak
    ABSTRACT Background, Adults with growth hormone deficiency (AGHD) have an adverse body composition with an increased prevalence of obesity. It is not known whether growth hormone replacement (GHR) results in alterations in energy intake (EI) and/or energy expenditure (EE). The aim of the study was to investigate the effects of GHR on EI and EE. Materials and methods, Nineteen hypopituitary adults (14 males, 5 females, mean age 46·2 years) with severe GHD (peak GH response to glucagon , 9 mU L,1) were studied. All patients self-injected recombinant human GH starting with 0·3 mg s.c. daily. The following were measured before and following 6 months of stable maintenance of GHR: food intake during a test meal, appetite ratings, resting EE (indirect calorimetry) and voluntary physical activity (accelerometry). Results, GHR nearly doubled voluntary physical activity (mean activity units 3319 vs. 1881, P = 0·007) and improved quality of life score (mean score 9·1 vs. 16·5, P < 0·0001). Subjects reported higher fasting hunger ratings (mean 64·8 vs. 49·6, P = 0·02) but ad libitum energy intake remained unchanged. Eating behavioural traits were favourably altered with lower disinhibition (mean 6·0 vs. 7·2, P = 0·02) and lower susceptibility to hunger ratings (4·6 vs. 6·8, P = 0·001) after GHR. Additionally, GHR did not result in significant changes in resting EE, body weight and body mass index. Conclusions, GHR in AGHD significantly improves voluntary physical activity and quality of life. Following GHR, subjects experience greater ,state' (physiological) hunger, reductions in eating disinhibition and hunger susceptibility, but no effects on calorie intake or macronutrient choice were detected. [source]

    Endocrine Function Is Altered in Chronic Migraine Patients with Medication-Overuse

    HEADACHE, Issue 4 2006
    Innocenzo Rainero MD
    Objective.,To evaluate the effects of analgesic overuse on endocrine function in patients with chronic migraine and medication-overuse headache (CM-MOH). Background.,Chronic migraine is frequently associated with an overuse of symptomatic medications. Drugs currently used in acute migraine attacks are associated with several endocrine effects. At present, the endocrine effects of medication overuse in chronic migraine patients are unknown. Methods.,Eighteen patients with CM-MOH, diagnosed according to the ICHD-II criteria, and 18 healthy controls received an intravenous administration of GHRH, hCRH, and TRH. Plasma concentrations of GH, TSH, ACTH, and cortisol were measured for a 90-minute period after administration of the specific releasing hormones. Results.,Hormonal basal concentrations were similar in both groups. GH response to GHRH was significantly reduced in patients with CM-MOH in comparison with controls. TRH induced a reduction of TSH concentrations only at the end of the test. After hCRH administration, ACTH and cortisol concentrations were significantly higher in cases than in controls. A significant correlation between duration of the disease and altered hormonal response was found. Conclusions.,Our study shows that both corticotropic and somatotropic functions are significantly impaired in CM-MOH patients and suggests a role for hormones in the development of chronic migraine. [source]

    Arginine test is not reliable for diagnosing cerebellar multiple system atrophy

    ANNALS OF NEUROLOGY, Issue 3 2010
    Raquel C. Gardner MD
    We evaluated the arginine growth hormone (GH) stimulation test for the diagnosis of cerebellar-type multiple system atrophy (MSAc) in patients with ataxia. Fourteen subjects with MSAc, 11 with idiopathic late-onset cerebellar ataxia (ILOCA), 10 with familial ataxia, and 10 healthy controls were tested. After pituitary GH deficiency was excluded, subjects underwent arginine testing. Peak serum GH response was analyzed. No significant differences in peak GH response were found between subject populations. Thirty-three percent of MSAc subjects mounted responses >10,g/l GH. Thirty-six percent of ILOCA subjects and 40 percent of healthy controls mounted responses <4,g/l GH. Arginine thus appears to be unreliable for the diagnosis of MSAc. ANN NEUROL 2010;67:404,408 [source]

    Dynamics of GH secretion during incremental exercise in obesity, before and after a short period of training at different work-loads

    CLINICAL ENDOCRINOLOGY, Issue 4 2010
    Alberto Salvadori
    Summary Background, Growth hormone (GH) secretion is normally sensitive to physical exercise. Intensity and duration of exercise, fitness and age can all influence the GH response to exercise. In obesity, GH secretion is decreased both in basal conditions and in response to exercise. Objective, To analyse the dynamics of GH response to a progressive cycloergometric test, conducted up to exhaustion, in adult normal subjects and obese patients, after a reconditioning program at different workloads. Design and methods, We studied eight lean subjects (four men, mean age 34·3 years, range 26,47 years, mean body mass index (BMI) 22·1 kg/m2). GH was sampled at baseline and during the last 30 s of each power output increase. Anaerobic threshold (AT) was detected by the V-slope method. The same test was carried out in 16 obese subjects (seven men, mean age 39·1 years, range 20,59 years, mean BMI 35·8 kg/m2) and repeated after a 4-week reconditioning program consisting of aerobic workout (Group A, eight subjects, three men, mean age 40·5 years, range 22,59 years, mean BMI 33·6 kg/m2), and aerobic plus anaerobic work (group B, eight subjects, four men, mean age 37·6 years, range 20,56 years, mean BMI 38·0 kg/m2) for 6 days/week, with no dietary restrictions. Results, Mean exercise peak occurred at higher intensity in controls (140 vs 110 W, P < 0·05), and AT exceeded at higher work outputs than in obese subjects (102 vs 74 W, P < 0·05). In controls, GH response to exercise was prompt and further sustained after AT; in obese subjects, GH increased slowly and insignificantly before AT, thereafter it increased to lower levels than in controls (P < 0·001). Following the reconditioning period, both Group A and Group B of obese subjects failed to improve exercise performance as well as GH response to exercise before AT; beyond AT, a greater GH response to exercise occurred in Group B than Group A (7·59 ± 0·32 ,g/l at peak of exercise) with significantly different Delta AUCs (Area Under the Curves) following AT: 30·5 ± 12 ,g.min/l in Group A vs 124·2 ± 38 ,g.min/l in Group B, P < 0·05. Conclusions Our results confirm the blunted GH response to exercise in obese adults when compared to lean counterparts. With obesity, aerobic training poorly increases the GH response beyond AT, while supplemental anaerobic workload appears to increase GH response beyond AT. These observations may have implications for the prescription of physical exercise, which is one of the recommendations in the management of obesity. [source]

    Ghrelin does not regulate the GH response to insulin-induced hypoglycaemia in children but could be involved in the regulation of cortisol secretion

    CLINICAL ENDOCRINOLOGY, Issue 1 2007
    J. Huber
    Summary Objective, Ghrelin activates the growth hormone secretagogue receptor GHS-R. It strongly stimulates GH secretion and has a role in energy homeostasis. The relationship between plasma ghrelin and cortisol levels during insulin-induced hypoglycaemia in prepubertal and pubertal children has not yet been investigated. The aim of the present study was to establish whether insulin-induced hypoglycaemia stimulates ghrelin secretion and whether changes in ghrelin concentrations are related to changes in GH and cortisol in children. Design and patients, We studied a group of 20 children and adolescents (five girls, 15 boys, mean age 10·8 ± 3·7 years) undergoing insulin tolerance tests (ITTs) for clinical investigation of GH deficiency. Measurements, Stimulation tests were performed to investigate the relationship between ghrelin, GH, cortisol and glucose levels according to age and pubertal stage by determining the ghrelin profiles during insulin-induced hypoglycaemia (at 0, 60 and 120 min). Results, Ghrelin was significantly and inversely related to body weight, height, body mass index (BMI) and age of children (P < 0·05). Significant changes in ghrelin levels (P = 0·00013) were found after the insulin bolus, with a decline at 60 min and an increase to baseline values at 120 min. Changes in cortisol levels were negatively correlated with changes in ghrelin at 60 min (r = ,0·59, P = 0·004) and at 120 min (r = ,0·605, P = 0·003). Conclusions, This study shows that ghrelin might not regulate the GH response to insulin-induced hypoglycaemia in prepubertal and pubertal children. A role for ghrelin in the regulation of cortisol secretion can be hypothesized concerning the negative correlation between changes in ghrelin and cortisol. Furthermore, the results imply that ghrelin secretion is age dependent and is a function of growth. [source]

    Effect of obesity and morbid obesity on the growth hormone (GH) secretion elicited by the combined GHRH + GHRP-6 test

    CLINICAL ENDOCRINOLOGY, Issue 6 2006
    Fahrettin Kelestimur
    Summary Objective, Obesity is characterized by low basal levels of growth hormone (GH) and impeded GH release. However, the main problem arises in the diagnosis of GH deficiency in adults, as all accepted cut-offs in the diagnostic tests of GH reserve are no longer valid in obese subjects. In this work, the role of obesity in the GH response elicited by the GHRH + GHRP-6 test was assessed in a large population of obese and nonobese subjects. Patients, GHRH + GHRP-6-induced GH peaks were evaluated in 542 subjects. One hundred and five were healthy obese, 50 were morbid obese, and 261 were nonobese (both normal weight and overweight). One hundred and seventy-six GH-deficient patients (obese and nonobese) were also studied. Results, A regression analysis of the 366 subjects with normal pituitary function indicated that adiposity had a negative effect on the elicited GH peak (r = ,0·503, P < 0·0001). A receiver operating characteristic (ROC) curve analysis showed that in subjects with a BMI 35, the currently accepted cut-offs of the GHRH + GHRP-6 test (GH peaks 20 µg/l: normal secretion; GH peaks 10 µg/l: GH deficiency), were fully operative. However, in subjects with a BMI > 35, normality was indicated by GH peaks 15 µg/l and GH deficiency by peaks 5 µg/l (1 µg/l = 2·6 mU/l). Conclusions, This study confirms: (a) that the combined provocative test is adequate to separate normal and GH-deficient subjects; (b) the negative effect of obesity on GH secretion; (c) that obesity accounts for 25% of the reduction of GH release; and (d) that present cut-off values are applicable to normal weight, overweight and grade I obesity subjects, whereas in obese subjects with a BMI exceeding 35, all the normative limits of the GHRH-GHRP +6 test must be reduced by 5 µg/l. [source]

    Lipid profiles in untreated severe congenital isolated growth hormone deficiency through the lifespan

    CLINICAL ENDOCRINOLOGY, Issue 1 2002
    Helena K. Gleeson
    Summary objective Growth hormone deficiency (GHD) is associated with adverse changes in lipid profile. However, changes in lipids through life in a homogeneous group of GHD subjects have not been defined. patients and measurements We examined lipid levels in a group of untreated severely GHD patients with a mutation in the GHRH receptor gene from a rural community in North-east Brazil. Lipid profiles in 15 GHD subjects [eight children and adolescents (one male), age (median [range]) 13·2 (5·4,19·9) years; seven adults (one male), age 47 (33,66) years] were compared with those in 29 indigenous controls from the same extended kindred [17 children and adolescents (six male), age 10·2 (5·3,18·4) years; 12 adults (eight male), age 54·5 (33,80) years]. All GHD subjects had a peak GH response of < 0·5 ng/ml in response to an insulin tolerance test and extremely reduced IGF-1 levels (median 5·5 ng/ml). Data were compared between cohorts and with an age- and sex-matched white American reference population. results Abnormalities were confined to plasma total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels. More GHD children had levels of plasma TC and LDL-C above the 95th percentile for our reference population (3/8 and 4/7, respectively) compared to controls (0/17 and 1/15, respectively) (P < 0·05). In the adults, median TC and LDL-C levels were higher in the GHD than controls (P < 0·05) (6·3 vs. 4·1 mmol/l; 4·4 vs. 2·7 mmol/l, respectively). Median Z -scores, calculated using values from the reference population, were not different between GHD children and adults for both TC (+0·8 vs.+0·4) and LDL-C (+1·4 vs.+0·7). conclusions The lipid profile in children as well as in adults with very severe GHD is adversely modified. There would appear to be no significant worsening of the lipid abnormality with duration of GHD or achievement of adulthood. [source]

    Endocrine responses to ghrelin in adult patients with isolated childhood-onset growth hormone deficiency

    CLINICAL ENDOCRINOLOGY, Issue 6 2002
    Gianluca Aimaretti
    Summary objective Ghrelin, a 28 amino acid acylated peptide, is a natural ligand of the GH secretagogues (GHS) receptor (GHS-R), which is specific for synthetic GHS. Similar to synthetic GHS, ghrelin strongly stimulates GH secretion but also displays significant stimulatory effects on lactotroph and corticotroph secretion. It has been hypothesized that isolated GH deficiency (GHD) could reflect hypothalamic impairment that would theoretically involve defect in ghrelin activity. patients In the present study, we verified the effects of ghrelin (1 µg/kg i.v.) on GH, PRL, ACTH and cortisol levels in adult patients with isolated severe GHD [five males and one female, age (mean ± SEM) 24·7 ± 2·6 years, BMI 25·7 ± 2·7 kg/m2]. In all patients, the GH response to insulin-induced hypoglycaemia (ITT, 0·1 IU regular insulin i.v.) and GH releasing hormone (GHRH) (1 µg/kg i.v.) + arginine (ARG, 0·5 g/kg i.v.) was also studied. The hormonal responses in GHD were compared with those in age-matched normal subjects (NS, seven males, age 28·6 ± 2·9 years, BMI 22·1 ± 0·8 kg/m2). results IGF-I levels in GHD were markedly lower than in NS (69·8 ± 11·3 vs. 167·9 ± 19·2 µg/l, P < 0·003). Ghrelin administration induced significant increase in GH, PRL, ACTH and cortisol levels in all GHD. In GHD, the GH response to ghrelin was higher (P < 0·05) than that to GHRH + ARG, which, in turn, was higher (P < 0·05) than that to ITT (9·2 ± 4·1 vs. 5·3 ± 1·7 vs. 1·4 ± 0·4 µg/l). These GH (1 µg/l = 2 mU/l) responses in GHD were markedly lower (P < 0·0001) than those in NS (ghrelin vs. GHRH + ARG vs. ITT 92·1 ± 16·7 vs. 65·3 ± 8·9 vs. 17·7 ± 3·5 µg/l). In GHD, the highest individual peak GH response to ghrelin was markedly lower than the lowest peak GH response in NS (28·5 vs. 42·9 µg/l). GHD and NS showed overlapping PRL (1 µg/l = 32 mU/l) (10·0 ± 1·4 vs. 14·9 ± 2·2 µg/l), ACTH (22·3 ± 5·3 vs. 18·7 ± 4·6 pmol/l) and cortisol responses (598·1 ± 52·4 vs. 486·9 ± 38·9 nmol/l). conclusions This study shows that ghrelin is one of the most powerful provocative stimuli of GH secretion, even in those patients with isolated severe GHD. In this condition, however, the somatotroph response is markedly reduced while the lactotroph and corticotroph responsiveness to ghrelin is fully preserved, indicating that this endocrine activity is fully independent of mechanisms underlying the GH-releasing effect. These results do not support the hypothesis that ghrelin deficiency is a major cause of isolated GH deficiency but suggest that ghrelin might represent a reliable provocative test to evaluate the maximal GH secretory capacity provided that appropriate cut-off limits are assumed. [source]

    Increased insulin sensitivity in young, growth hormone deficient children

    CLINICAL ENDOCRINOLOGY, Issue 1 2001
    Sandra Husbands
    OBJECTIVE Although growth hormone (GH) has well documented insulin antagonistic effects, GH deficient adults often demonstrate insulin resistance. In young GH deficient children, increased susceptibility to hypoglycaemia might indicate increased insulin sensitivity; however, this has not been documented. We therefore determined insulin sensitivity in GH deficient and GH sufficient children. DESIGN AND PATIENTS Prospective study of children undergoing insulin tolerance tests for clinical investigation of GH or cortisol secretion at a regional Paediatric Endocrine/Growth Clinic between October 1986 and December 1997. Ninety-one tests were performed in children with GH deficiency and 142 tests in children with normal GH response to insulin (peak GH , 20 IU/l). MEASUREMENTS The standard insulin tolerance test was modified to permit frequent measurements of glucose (0, 5, 10, 15, 20, 30, 45, 60 and 90 minutes). Rate of log glucose disappearance in the first 15 minutes was calculated as a direct measure of insulin sensitivity. RESULTS GH deficient children were more insulin sensitive than GH sufficient children (P = 0·004) and had lower glucose nadirs post-insulin (P = 0·005). Subgroup analysis revealed that these differences were greater in younger (< 12 years old) or pre/early pubertal children. In 14 prepubertal children, exogenous sex steroid priming resulted in lower insulin sensitivity (P < 0·05) compared to nonprimed tests. CONCLUSIONS Young GH deficient children were more insulin sensitive than children with normal GH secretion. This difference attenuated with age and puberty, possibly secondary to pubertal sex steroids; however, insulin resistance as reported in GH deficient adults, was not observed in adolescents. [source]

    Skeletal Growth Acceleration with Growth Hormone Secretagogues in Transgenic Growth Retarded Rats: Pattern-Dependent Effects and Mechanisms of Desensitization

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 6 2001
    T. Wells
    Abstract The transgenic growth retarded (Tgr) rat is the first genetic model of growth hormone (GH) deficiency whose growth can be accelerated with exogenous GH secretagogues (GHSs). In this study, we have demonstrated that GHS-receptor (GHS-R) mRNA expression in the arcuate nucleus of Tgr rats was not significantly different to that in wild-type littermates. We have confirmed that GHS-induced elevation in body weight gain was accompanied by acceleration of skeletal growth, and that the effects of the GHS, GHRP-6, were both dose- and pattern-dependent. The growth response with continuous infusion of GHRP-6 was transient, accompanied by suppression of GH and corticosterone responses to bolus injection of GHRP-6. This desensitization occurred without downregulation of arcuate GHS-R mRNA expression, but was accompanied by elevated periventricular somatostatin mRNA expression. In contrast, pulsatile (3-hourly) infusion of GHRP-6 produced sustained growth and GH responses, which were accompanied by suppression of corticosterone responses and elevated arcuate GH-releasing factor (GRF) mRNA expression. Skeletal growth was further accelerated by coinfusion of GRF, but significant depletion of pituitary GH stores suggested that this growth rate may not be sustainable. These experiments confirm the importance of the Tgr rat for investigating the growth promoting potential of the GHSs in the context of GH-deficient dwarfism, and suggest that elevated somatostatin expression may mediate the suppression of the GRF-GH and hypothalamo-pituitary-adrenal axes following continuous GHRP-6 treatment. [source]