scholarly journals Differential Effects of GH Replacement on the Components of the Leptin System in GH-Deficient Individuals

2002 ◽  
Vol 87 (2) ◽  
pp. 798-804 ◽  
Author(s):  
Harpal S. Randeva ◽  
Robert D. Murray ◽  
Krzysztof C. Lewandowski ◽  
Chris J. O’Callaghan ◽  
Rudiger Horn ◽  
...  
Keyword(s):  
Body Composition ◽  
Fat Mass ◽  
Leptin Receptor ◽  
Negative Relationship ◽  
Direct Result ◽  
Gh Treatment ◽  
Serum Leptin ◽  
Soluble Leptin Receptor ◽  
Igf I ◽  
Leptin System

GH therapy is associated with a reduction in fat mass and an increase in lean mass in subjects with GH deficiency (GHD). Leptin, like GH, plays an important role in the regulation of body composition. GH treatment has been shown to reduce serum leptin; however, the physiological interactions between the leptin system (free leptin, bound leptin, and soluble leptin receptor) and the GH/IGF-I system largely remain unknown.Twenty-five patients with childhood (n = 10) and adult-onset (n = 15) GHD were studied. GH status had previously been determined using an insulin tolerance test and/or an arginine stimulation test. The following parameters were recorded at baseline (V1) and then after 3 months (V2) and 6 months (V3) on GH treatment: fat mass, body mass index (BMI), and waist/hip ratio (WHR); blood samples were taken after an overnight fast for free leptin, bound leptin, soluble leptin receptor, insulin, and IGF-I.At V2 and V3, respectively, a fall in free leptin (P < 0.001 for each), and at V3 a fall in in percent fat mass (P < 0.001) were observed. There were no significant changes in BMI or WHR. Simultaneously, there was a rise in insulin (P = 0.068 and P < 0.001), IGF-I (P < 0.001 and P < 0.001), bound leptin (P = 0.005 and P < 0.001), and soluble leptin receptor (P = 0.61 and P < 0.001). A positive relationship was noted between free leptin and BMI (P < 0.001) and between free leptin and fat mass (P < 0.001), and a negative relationship was found between free leptin and IGF-I (P < 0.001) and, within patient, between free leptin and insulin (P < 0.001). There was no significant correlation between free leptin and WHR. Bound leptin had a positive association with IGF-I (P < 0.001) and insulin (P = 0.002) and a negative relationship with percent fat mass (P = 0.023). Soluble leptin receptor was also positively related to IGF-I (P < 0.001).In conclusion, our data suggest that the reduction in serum leptin with GH treatment, as noted by others, is mediated through a fall in free leptin. The fall in free leptin and in part the rise in bound leptin are most likely through a reduction in percent fat mass. However, the observed changes in free leptin and bound leptin and, more importantly, the rise in soluble leptin receptor, are not explained entirely by modifications in body composition and may be a direct result of GH/IGF-I.

Effect of growth hormone treatment on hormonal parameters, body composition and strength in athletes

1993 ◽  
Vol 128 (4) ◽  
pp. 313-318 ◽  
Author(s):  
Roman Deyssig ◽  
Herwig Frisch ◽  
Werner F Blum ◽  
Thomas Waldhör
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Body Fat ◽  
Fat Mass ◽  
Binding Protein ◽  
Controlled Study ◽  
Gh Treatment ◽  
Igf I ◽  
Igf Binding ◽  
Igf Binding Protein

The effect of recombinant GH on strength, body composition and endocrine parameters in power athletes was investigated in a controlled study. Twenty-two healthy, non-obese males (age 23.4±0.5 years; ideal body weight 122±3.1%, body fat 10.1±1.0%; mean±sem) were included. Probands were assigned in a double-blind manner to either GH treatment (0.09U (kg BW)−1 day−1 sc) or placebo for a period of six weeks. To exclude concurrent treatment with androgenic-anabolic steroids urine specimens were tested at regular intervals for these substances. Serum was assayed for GH, IGF-I, IGF-binding protein, insulin and thyroxine before the onset of the study and at two-weekly intervals thereafter. Maximal voluntary strength of the biceps and quadriceps muscles was measured on a strength training apparatus. Fat mass and lean body mass were derived from measurements of skinfolds at ten sites with a caliper. For final evaluation only data of those 8 and 10 subjects in the two groups who completed the study were analyzed. GH, IGF-I and IGF-binding protein were in the normal range before therapy and increased significantly in the GH-treated group. Fasting insulin concentrations increased insignificantly and thyroxine levels decreased significantly in the GH-treated probands. There was no effect of GH treatment on maximal strength during concentric contraction of the biceps and quadriceps muscles. Body weight and body fat were not changed significantly during treatment. We conclude that the anabolic, lipolytic effect of GH therapy in adults depends on the degree of fat mass and GH deficiency. In highly trained power athletes with low fat mass there were no effects of GH treatment on strength and body composition.

scholarly journals Effects of Growth Hormone (GH) on Ghrelin, Leptin, and Adiponectin in GH-Deficient Patients

2003 ◽  
Vol 88 (11) ◽  
pp. 5193-5198 ◽  
Author(s):  
Britt Edén Engström ◽  
Pia Burman ◽  
Camilla Holdstock ◽  
F. Anders Karlsson
Keyword(s):  
Body Composition ◽  
Body Fat ◽  
Fat Mass ◽  
Glucose Production ◽  
Serum Levels ◽  
Fat Free Mass ◽  
Metabolic Effects ◽  
Controlled Study ◽  
Gh Treatment ◽  
Igf I

Abstract Ghrelin is a recently discovered gastric peptide that increases appetite, glucose oxidation, and lipogenesis and stimulates the secretion of GH. In contrast to ghrelin, GH promotes lipolysis, glucose production, and insulin secretion. Both ghrelin and GH are suppressed by intake of nutrients, especially glucose. The role of GH in the regulation of ghrelin has not yet been established. We investigated the effect of GH on circulating levels of ghrelin in relation to its effects on glucose, insulin, body composition, and the adipocyte-derived peptides leptin and adiponectin. Thirty-six patients with adult-onset GH deficiency received recombinant human GH for 9 months in a placebo-controlled study. Body composition and fasting serum analytes were assessed at baseline and at the end of the study. The GH treatment was accompanied by increased serum levels of IGF-I, reduced body weight (−2%) and body fat (−27%), and increased serum concentrations of glucose (+10%) and insulin (+48%). Ghrelin levels decreased in 30 of 36 subjects by a mean of −29%, and leptin decreased by a mean of −24%. Adiponectin increased in the women only. The decreases in ghrelin and leptin correlated with changes in fat mass, fat-free mass, and IGF-I. The reductions in ghrelin were predicted independently of the changes in IGF-I and fat mass. It is likely that the reductions in ghrelin and leptin reflect the metabolic effects of GH on lipid mobilization and glucose production. Possibly, a suppression of ghrelin promotes loss of body fat in GH-deficient patients receiving treatment. The observed correlation between the changes in ghrelin and IGF-I may suggest that the GH/IGF-I axis has a negative feedback on ghrelin secretion.

scholarly journals Changes in body composition and leptin levels during growth hormone (GH) treatment in short children with various GH secretory capacities

1999 ◽  
pp. 35-42 ◽  
Author(s):  
H Matsuoka ◽  
H Fors ◽  
I Bosaeus ◽  
S Rosberg ◽  
K Albertsson-Wikland ◽  
...  
Keyword(s):  
Body Composition ◽  
Body Fat ◽  
Fat Mass ◽  
Gh Treatment ◽  
Deconvolution Analysis ◽  
Serum Leptin ◽  
Gh Secretion ◽  
Short Children ◽  
Total Body Fat ◽  
Total Body

OBJECTIVE: The aim of this study was to follow changes in body composition, estimated by dual-energy X-ray absorptiometry (DXA), in relation to changes in leptin during the first year of GH therapy in order to test the hypothesis that leptin is a metabolic signal involved in the regulation of GH secretion in children. DESIGN AND METHODS: In total, 33 prepubertal children were investigated. Their mean (S.D.) chronological age at the start of GH treatment was 11.5 (1.6) years, and their mean height was -2.33 (0.38) S.D. scores (SDS). GH was administered subcutaneously at a daily dose of 0.1 (n=26) or 0.2 (n=7) IU/kg body weight. Ten children were in the Swedish National Registry for children with GH deficiency, and twenty-three children were involved in trials of GH treatment for idiopathic short stature. Spontaneous 24-h GH secretion was studied in 32 of the children. In the 24-h GH profiles, the maximum level of GH was determined and the secretion rate estimated by deconvolution analysis (GHt). Serum leptin levels were measured at the start of GH treatment and after 10 and 30 days and 3, 6 and 12 months of treatment. Body composition measurements, by DXA, were performed at baseline and 12 months after the onset of GH treatment. RESULTS: After 12 months of GH treatment, mean height increased from -2.33 to -1.73 SDS and total body fat decreased significantly by 3.0 (3.3)%. Serum leptin levels were decreased significantly at all time points studied compared with baseline. There was a significant correlation between the change in total body fat and the change in serum leptin levels during the 12 months of GH treatment, whereas the leptin concentration per unit fat mass did not change. In a multiple stepwise linear regression analysis with 12 month change in leptin levels as the dependent variable, the percentage change in fat over 12 months, the baseline fat mass (%) of body mass and GHt accounted for 24.0%, 11.5% and 12.2% of the variability respectively. CONCLUSIONS: There are significant correlations between changes in leptin and fat and endogenous GH secretion in short children with various GH secretory capacities. Leptin may be the messenger by which the adipose tissue affects hypothalamic regulation of GH secretion.

scholarly journals Are serum leptin and the Gln223Arg polymorphism of the leptin receptor determinants of bone homeostasis in elderly men?

2006 ◽  
Vol 154 (5) ◽  
pp. 707-714 ◽  
Author(s):  
Patricia Crabbe ◽  
Stefan Goemaere ◽  
Hans Zmierczak ◽  
Inge Van Pottelbergh ◽  
Dirk De Bacquer ◽  
...  
Keyword(s):  
Body Composition ◽  
Fat Mass ◽  
Leptin Receptor ◽  
Type I ◽  
Bone Homeostasis ◽  
Mineral Density ◽  
Elderly Men ◽  
Cross Sectional ◽  
Serum Leptin ◽  
Free Estradiol

Objective: Across studies it has been suggested that leptin intervenes as a regulator of bone metabolism. This study assesses the contribution in elderly men of leptin and the Gln223Arg leptin receptor gene (LEPR) polymorphism to the variation in bone homeostasis, in relation to body composition and free estradiol as major confounders. Design: We performed cross-sectional (n = 270) and longitudinal (mean follow-up 3.4 years, n = 214) evaluations in elderly men. Methods: Serum leptin, LEPR genotype, baseline bone mineral density (BMD), longitudinal BMD changes at the hip and forearm, and biochemical markers of bone turnover were determined. Results: In cross-sectional analyses absolute fat mass was the index of body composition most strongly associated with leptin (r = 0.74; P < 0.001). LEPR genotypes and serum leptin were not associated. Serum bone-specific alkaline phosphatase (S-BAP) was associated with LEPR genotypes (P = 0.05) and urinary C-terminal telopeptides of type I collagen (U-CTX) were associated with leptin levels (P = 0.03), independently from age, fat mass and free estradiol. Baseline BMD at the hip and forearm was neither associated with leptin nor with LEPR genotypes. Prospectively assessed BMD loss was not associated with serum leptin at the hip, whereas BMD loss was positively associated with leptin at the forearm (P = 0.01), independently from age, fat mass and free estradiol. Longitudinal changes in hip or forearm BMD were not associated with LEPR genotypes. Conclusion: The findings suggest a possible role for leptin as determinant of bone homeostasis in elderly men, but with only modest impact independently from body composition and free estradiol.

scholarly journals Serum Leptin Response to the Acute and Chronic Administration of Growth Hormone (GH) to Elderly Subjects with GH Deficiency1

1999 ◽  
Vol 84 (4) ◽  
pp. 1288-1295 ◽  
Author(s):  
Matthew S. Gill ◽  
Andrew A. Toogood ◽  
Jenny Jones ◽  
Peter E. Clayton ◽  
Stephen M. Shalet
Keyword(s):  
Body Composition ◽  
Median Time ◽  
Dual Energy ◽  
Significant Rise ◽  
Gh Treatment ◽  
Blood Samples ◽  
Serum Leptin ◽  
X Ray ◽  
Igf I ◽  
Igfbp 3

In human studies, the principal determinant of serum leptin concentrations is fat mass (FM), but lean mass (LM) also has a significant negative influence. GH treatment in GH deficiency (GHD) alters body composition, increasing LM and decreasing FM, and thus would be expected to alter leptin concentrations. We have therefore examined the acute and chronic effects of GH on serum leptin in 12 elderly GHD subjects (ages 62–85 yr; 3 women and 9 men). FM (kilograms) and LM (kilograms) were determined by dual energy x-ray absortiometry. Leptin, insulin, insulin-like growth factor I (IGF-I), IGF-II, IGF-binding protein-1 (IGFBP-1), IGFBP-2, and IGFBP-3 were measured by specific immunoassays. Leptin, insulin, and IGFBP-1 concentrations were log10 transformed, and data were expressed as the geometric mean (−1, +1 tolerance factor). All other data are presented as the mean ± sd.In the acute study, patients received a single bolus dose of GH (0.1 mg/kg BW) at time zero, with blood samples drawn at 0, 12, 24, 48, and 72 h and 1 and 2 weeks. There was a significant rise in leptin, insulin, and IGF-I at a median time of 24 h, followed by a significant fall, and nadir concentrations were reached at a median time of 1.5 weeks (leptin) or 2 weeks (insulin and IGF-I). IGFBP-3 concentrations were also significantly increased, but peak concentrations were not achieved until 48 h. IGF-II, IGFBP-1, and IGFBP-2 exhibited transient decreases before returning to baseline levels. There was no relationship between increased leptin concentrations and either insulin or IGF-I concentrations.In the chronic study, patients received daily GH treatment at doses of 0.17, 0.33, and 0.5 mg/day, each for 3 months (total time on GH, 9 months), and were then followed off GH for a further 3 months. Dual energy x-ray absortiometry was undertaken at 0, 3, 6, 9, and 12 months, and blood samples were drawn at these time points. Over 9 months on GH there was a significant fall in FM and a significant rise in LM, but no change in leptin. There were also significant increments in insulin, IGF-I, and IGFBP-3, whereas IGF-II, IGFBP-1, and IGFBP-2 did not change over 9 months of GH treatment. After 3 months off GH, there was a significant rise in FM and leptin.High dose single bolus GH led to an increase in serum leptin within 24 h apparently independent of changes in insulin or IGF-I. Despite the changes in body composition during chronic GH treatment, there was no change in leptin. However, discontinuation of GH led to a rapid reversal of the favorable body composition and a rise in serum leptin.

Effect of valproic acid treatment on body composition, leptin and soluble leptin receptor in epileptic children

2006 ◽  
Vol 37 (06) ◽  
Author(s):  
M Rauchenzauner ◽  
E Haberlandt ◽  
S Scholl-Bürgi ◽  
D Karall ◽  
E Schönherr ◽  
...  
Keyword(s):  
Valproic Acid ◽  
Body Composition ◽  
Acid Treatment ◽  
Leptin Receptor ◽  
Soluble Leptin Receptor ◽  
Epileptic Children

Effect of valproic acid treatment on body composition, leptin and the soluble leptin receptor in epileptic children

2008 ◽  
Vol 80 (2-3) ◽  
pp. 142-149 ◽  
Author(s):  
M. Rauchenzauner ◽  
E. Haberlandt ◽  
S. Scholl-Bürgi ◽  
D. Karall ◽  
E. Schoenherr ◽  
...  
Keyword(s):  
Valproic Acid ◽  
Body Composition ◽  
Acid Treatment ◽  
Leptin Receptor ◽  
Soluble Leptin Receptor ◽  
Epileptic Children

Gender differences in regional body composition and somatotrophic influences of IGF-I and leptin

2002 ◽  
Vol 92 (4) ◽  
pp. 1611-1618 ◽  
Author(s):  
Bradley C. Nindl ◽  
Charles R. Scoville ◽  
Kathleen M. Sheehan ◽  
Cara D. Leone ◽  
Robert P. Mello
Keyword(s):  
Gender Differences ◽  
Body Composition ◽  
Growth Factor ◽  
Soft Tissue ◽  
Fat Mass ◽  
Soft Tissue Mass ◽  
Insulin Like Growth Factor ◽  
Tissue Mass ◽  
Regional Body Composition ◽  
Igf I

This study evaluated the arm, trunk, and leg for fat mass, lean soft tissue mass, and bone mineral content (BMC) assessed via dual-energy X-ray absorptiometry in a group of age-matched (∼29 yr) men ( n = 57) and women ( n = 63) and determined their relationship to insulin-like growth factor I (IGF-I) and leptin. After analysis of covariance adjustment to control for differences in body mass between genders, the differences that persisted ( P ≤ 0.05) were for lean soft tissue mass of the arm (men: 7.1 kg vs. women: 6.4 kg) and fat mass of the leg (men: 5.3 kg vs. women: 6.8 kg). Men and women had similar ( P ≥ 0.05) values for fat mass of the arms and trunk and lean soft tissue mass of the legs and trunk. Serum IGF-I and insulin-like growth factor binding protein-3 correlated ( P≤ 0.05) with all measures of BMC ( r values ranged from 0.31 to 0.39) and some measures of lean soft tissue mass for women ( r = 0.30) but not men. Leptin correlated ( P≤ 0.05) similarly for measures of fat mass for both genders ( r values ranging from 0.74 to 0.85) and for lean soft tissue mass of the trunk ( r = 0.40) and total body ( r = 0.32) for men and for the arms in women ( r = 0.56). These data demonstrate that 1) the main phenotypic gender differences in body composition are that men have more of their muscle mass in their arms and women have more of their fat mass in their legs and 2) gender differences exist in the relationship between somatotrophic hormones and lean soft tissue mass.

scholarly journals Circulating Level of Soluble Leptin Receptor and its Association with Cardiometabolic Risk Factors among Obese Subjects in Kerala, South India

2021 ◽  
pp. 232-239
Author(s):  
K. S. Manju ◽  
K. B. Leena ◽  
L. Vijayalekshmi ◽  
K. T. Shenoy
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Cardiometabolic Risk ◽  
Leptin Receptor ◽  
Obese Group ◽  
Serum Leptin ◽  
Control Subjects ◽  
Soluble Leptin Receptor ◽  
Significant Difference ◽  
Obese Subjects

Background and Aims: Leptin, the peptide hormone secreted mainly by adipose tissue is reported to play the central role in the pathogenesis of obesity. Leptin exerts its biological effects through specific receptor molecules present in target tissues. Among the different isoforms of leptin receptor, the Soluble Leptin Receptor (SLR) is the major leptin binding protein seen in circulation which modulates the bioavailability of leptin. Our objectives were to analyse the level of circulating SLR among obese subjects and its association with biomarkers of obesity, serum leptin, insulin and cardiometabolic risk factors in comparison with healthy age and sex matched control subjects. Methods: About 173 study participants of both genders were selected and grouped as case (n=102) and control (n=71) with a cut off point of BMI 25kg/m2. Waist to hip ratio (WHR) and body fat percentage (BF%) were calculated from anthropometric measurements. Leptin, insulin, soluble leptin receptor were estimated in fasting blood samples by sandwich ELISA method. Fasting plasma glucose and lipid profile were measured by standard enzymatic methods in autoanalyzer. Homeostasis Model Assessment of Insulin resistance (HOMA-IR) was calculated. Comparison between groups was done by independent sample ‘t’ test. P values <.05 were considered statistically significant. Results: The SLR level was found to be increased in obese group in comparison with control group(P =.001). A significant increase in serum leptin and insulin level was observed in obese group when compared to control (P =.001). Obese group showed more than two fold increase in insulin resistance expressed as HOMA-IR when compared to control subjects (P =.001). But no significant difference in the synthesis of insulin expressed as HOMA-beta between the groups. No significant difference in serum lipoprotein levels was observed between the two groups. Conclusion: Increased level of circulating soluble leptin receptor has been observed in obese subjects in comparison with control subjects and is associated with hyperleptinemia, hypertension and insulin resistance.

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