Growth hormone treatment of obese women for 5 wk: effect on body composition and adipose tissue LPL activity

Richelsen, Bjørn; Pedersen, Steen; Børglum, Jens; Møller‐Pedersen, Torben; Jørgensen, J. O. L.

doi:10.1152/ajpendo.1994.266.2.e211

Cited by 87 publications

(106 citation statements)

References 24 publications

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“…The findings reported here are not unprecedented, since improved glucose metabolism has been described in three of 24 clinical trials [5][6][7]. However, many studies report that growth hormone treatment of obesity has either little to no effect [8,9,11,12] or negative effects [31][32][33][34] on glucose metabolism. A recent metaanalysis comparing 24 studies in which growth hormone was used to treat obesity revealed a small increase in fasting plasma glucose and fasting insulin [35].…”

Section: Discussionsupporting

confidence: 47%

Growth hormone improves body composition, fasting blood glucose, glucose tolerance and liver triacylglycerol in a mouse model of diet-induced obesity and type 2 diabetes

et al. 2009

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Aims/hypothesis Growth hormone has been used experimentally in two studies to treat individuals with type 2 diabetes, with both reporting beneficial effects on glucose metabolism. However, concerns over potential diabetogenic actions of growth hormone complicate its anticipated use to treat type 2 diabetes. Thus, an animal model of type 2 diabetes could help evaluate the effects of growth hormone for treating this condition. Methods Male C57BL/6J mice were placed on a high-fat diet to induce obesity and type 2 diabetes. Starting at 16 weeks of age, mice were treated once daily for 6 weeks with one of four different doses of growth hormone. Body weight, body composition, fasting blood glucose, insulin, glucose tolerance, liver triacylglycerol, tissue weights and blood chemistries were determined. Results Body composition measurements revealed a dosedependent decrease in fat and an increase in lean mass. Analysis of fat loss by depot revealed that subcutaneous and mesenteric fat was the most sensitive to growth hormone treatment. In addition, growth hormone treatment resulted in improvement in glucose metabolism, with the highest dose normalising glucose, glucose tolerance and liver triacylglycerol. In contrast, insulin levels were not altered by the treatment, nor did organ weights change. However, fasting plasma leptin and resistin were significantly decreased after growth hormone treatment. Conclusions/interpretation Growth hormone therapy improves glucose metabolism in this mouse model of obesity and type 2 diabetes, providing a means to explore the molecular mechanism(s) of this treatment.

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Section: Discussionsupporting

confidence: 47%

Growth hormone improves body composition, fasting blood glucose, glucose tolerance and liver triacylglycerol in a mouse model of diet-induced obesity and type 2 diabetes

et al. 2009

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“…19 This is consistent with the failure of GH treatment to signi®cantly enhance diet-induced fat loss in obese patients observed in other studies 9,10,12 with the exception of a recent one 27 in which the patients received an energy intake (62.79 kJ/kg IBW daily) 50% higher than the one adopted in our protocol. A more striking decrease in body fat, especially at visceral level, 28 is well documented in obese patients receiving GH while on a normocaloric diet. 13,28,29 The observation of a smaller LBM loss in GHtreated women in spite of no signi®cant differences in changes of body weight and fat mass between the two groups may not be in contradiction; in fact, statistically insigni®cant but not negligible variations in parameters of body composition may account for the apparent discrepancy of these results.…”

Section: Discussionmentioning

confidence: 94%

“…A more striking decrease in body fat, especially at visceral level, 28 is well documented in obese patients receiving GH while on a normocaloric diet. 13,28,29 The observation of a smaller LBM loss in GHtreated women in spite of no signi®cant differences in changes of body weight and fat mass between the two groups may not be in contradiction; in fact, statistically insigni®cant but not negligible variations in parameters of body composition may account for the apparent discrepancy of these results. The good correspondence between body weight loss estimated by Growth hormone treatment in obesity M Tagliaferri et al DEXA (sum of fat mass and LBM losses) and body weight estimated using a balance gives consistency to the data.…”

Section: Discussionmentioning

confidence: 94%

Metabolic effects of biosynthetic growth hormone treatment in severely energy-restricted obese women

et al. 1998

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OBJECTIVE: Severe energy restriction in the treatment of obesity is limited by catabolism of body protein stores and, consequently, loss of lean as well as fat tissue. Growth hormone (GH), whose secretion is markedly impaired in obesity, is endowed with both lipolytic and protein anabolic properties. The aim of this study was to verify the effects of GH administration on body composition, plasma leptin levels and energy metabolism in obese patients undergoing severe dietary restriction. DESIGN: Single-blind placebo-controlled study. Twenty obese women were fed a diet of 41.86 kJ/kg ideal body weight (IBW) daily for 4 weeks: 10 of them were randomly assigned to a 4 week treatment with biosynthetic GH (rhGH, Saizen, Serono, Rome, Italy), 1 U/kg IBW/week in daily subcutaneous injections; the other 10 patients, matched for age and BMI, received vehicle only. SUBJECTS: Twenty women with simple obesity (age: 25.4 AE 1.07 y, BMI: 35.9 AE 0.35 kg/m 2 ). MEASUREMENTS: Plasma IGF-I and leptin, serum markers of bone turnover (serum bone isoenzyme of alkaline phosphatase, osteocalcin and urinary hydroxyproline), nitrogen balance, body composition (by DEXA), and resting energy expenditure (REE, by indirect calorimetry) were evaluated at baseline and after 4 weeks. RESULTS: Mean IGF-I plasma levels, not in¯uenced by energy restriction in patients receiving placebo, displayed a signi®cant increase in the group treated with rhGH. The mean weight reduction and fat mass loss were not signi®cantly different in the two groups (6.0 AE 0.51 vs 7.2 AE 0.30 kg, NS, and 5.36 AE 0.460 vs 4.28 AE 0.572 kg, NS, with rhGH and placebo, respectively). Likewise, plasma leptin levels decreased signi®cantly in weight-reduced subjects receiving either rhGH (from 16.2 AE 2.37 to 6.4 AE 0.39 ng/ml, P`0.05) or placebo (from 14.3 AE 2.55 to 7.7 AE 3.77 ng/ml, P`0.05). On the contrary, the mean decrease of lean body mass (LBM) was signi®cantly lower in the GH-treated patients than in those receiving vehicle (1.52 AE 0.60 vs 3.79 AE 0.45 kg, P`0.05). In keeping with these ®ndings, the mean daily nitrogen balance was signi®cantly less negative in the GH-treated subjects than in the vehicle-injected patients (mean of the 4 week daily urine collections 7185.7 AE 40.33 vs 7363.9 AE 55.47 mmol/d, P`0.05, respectively). Further, a signi®cant reduction of mean REE was recorded in the energy-restricted placebo-treated patients (from 8807 AE 498 to 7580 AE 321 kJ/24 h, P`0.05), but not in the patients receiving rhGH (from 8367 AE 580 to 8903 AE 478 kJ/ 24 h, NS). Actually, when corrected for LBM, REE was even increased by GH administration (from 197.9 AE 11.76 to 219.3 AE 9.87 kJ/kg LBM/24 h, P`0.05), whereas it was unchanged in the placebo group (from 201.7 AE 13.85 to 190.0 AE 9.87 kJ/kg LBM/24 h, NS). A tendency of serum markers of bone turnover to increase was observed in the patients treated with rhGH, however with no changes in bone mineral content and density. CONCLUSION: rhGH treatment, though unable to enhance diet-induced weight and fat mass reduction...

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“…In contrast, a signi®cant decrease in body fat, especially at visceral level, 135,136 is well documented in obese patients receiving GH, while on a normocaloric diet. 45,135 ± 137 This ®nding is in line with the reduction of body fat observed in ad libitum fed, but not in calorie-restricted, beef steers after bovine GH administration.…”

Section: Effects Of Gh Administration On Body Composition In Obesitymentioning

confidence: 99%

“…Thus in a number of studies, GH administration displayed bene®cial effects on body composition in obese patients either on weight-maintaining diets 135,137 or undergoing both moderate 76,126 and severe 131,132 caloric restriction. GH administration to obese patients appears to be a safe treatment, although a few adverse effects have been reported in some trials.…”

Section: Effects Of Gh Administration On Body Composition In Obesitymentioning

confidence: 99%

Growth hormone in obesity

1999

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Growth hormone (GH) secretion, either spontaneous or evoked by provocative stimuli, is markedly blunted in obesity. In fact obese patients display, compared to normal weight subjects, a reduced half-life, frequency of secretory episodes and daily production rate of the hormone. Furthermore, in these patients GH secretion is impaired in response to all traditional pharmacological stimuli acting at the hypothalamus (insulin-induced hypoglycaemia, arginine, galanin, L-dopa, clonidine, acute glucocorticoid administration) and to direct somatotrope stimulation by exogenous growth hormone releasing hormone (GHRH). Compounds thought to inhibit hypothalamic somatostatin (SRIH) release (pyridostigmine, arginine, galanin, atenolol) consistently improve, though do not normalize, the somatotropin response to GHRH in obesity. The synthetic growth hormone releasing peptides (GHRPs) GHRP-6 and hexarelin elicit in obese patients GH responses greater than those evoked by GHRH, but still lower than those observed in lean subjects. The combined administration of GHRH and GHRP-6 represents the most powerful GH releasing stimulus known in obesity, but once again it is less effective in these patients than in lean subjects. As for the peripheral limb of the GH ± insulin-like growth factor I (IGF-I) axis, high free IGF-I, low IGF-binding proteins 1 (IGFBP-1) and 2 (IGFBP-2), normal or high IGFBP-3 and increased GH binding protein (GHBP) circulating levels have been described in obesity. Recent evidence suggests that leptin, the product of adipocyte speci®c ob gene, exerts a stimulating effect on GH release in rodents; should the same hold true in man, the coexistence of high leptin and low GH serum levels in human obesity would ®t in well with the concept of a leptin resistance in this condition. Concerning the in¯uence of metabolic and nutritional factors, an impaired somatotropin response to hypoglycaemia and a failure of glucose load to inhibit spontaneous and stimulated GH release are well documented in obese patients; furthermore, drugs able to block lipolysis and thus to lower serum free fatty acids (NEFA) signi®cantly improve somatotropin secretion in obesity. Caloric restriction and weight loss are followed by the restoration of a normal spontaneous and stimulated GH release. On the whole, hypothalamic, pituitary and peripheral factors appear to be involved in the GH hyposecretion of obesity. A SRIH hypertone, a GHRH de®ciency or a functional failure of the somatotrope have been proposed as contributing factors. A lack of the putative endogenous ligand for GHRP receptors is another challenging hypothesis. On the peripheral side, the elevated plasma levels of NEFA and free IGF-I may play a major role. Whatever the cause, the defect of GH secretion in obesity appears to be of secondary, probably adaptive, nature since it is completely reversed by the normalization of body weight. In spite of this, treatment with biosynthetic GH has been shown to improve the body composition and the metabolic ef®cacy of lean body mass in obese pa...

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Growth hormone treatment of obese women for 5 wk: effect on body composition and adipose tissue LPL activity

Cited by 87 publications

References 24 publications

Growth hormone improves body composition, fasting blood glucose, glucose tolerance and liver triacylglycerol in a mouse model of diet-induced obesity and type 2 diabetes

Growth hormone improves body composition, fasting blood glucose, glucose tolerance and liver triacylglycerol in a mouse model of diet-induced obesity and type 2 diabetes

Metabolic effects of biosynthetic growth hormone treatment in severely energy-restricted obese women

Growth hormone in obesity

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