Effects of treatment with recombinant human growth hormone on insulin sensitivity and glucose metabolism in adults with growth hormone deficiency

Fowelin, J.; Attvall, Stig; Lager, I; Bengtsson, Bengt‐Åke

doi:10.1016/0026-0495(93)90197-v

Cited by 183 publications

(130 citation statements)

References 15 publications

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“…The effect of GH replacement therapy on insulin sensitivity appears to be biphasic. After an initial deterioration during the first months of therapy, insulin sensitivity then improves and returns towards baseline values as seen in several studies (9,10). This improvement and return towards baseline values is probably due to the improved body composition by GH replacement with reduced total body fat and increased lean body mass (10).…”

Section: Insulin Sensitivitymentioning

confidence: 85%

Safety aspects of GH replacement

Svensson¹,

Bengtsson²

2009

European Journal of Endocrinology

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In adults, GH replacement therapy will often be maintained for decades. Owing to the long duration of GH replacement in many adults, it is essential to establish the long-term safety aspects of the treatment. In this review, studies that have investigated the safety profile of long-term GH replacement will be reviewed with an emphasis on studies based on data from the Pfizer International Metabolic Database (KIMS). These studies show that long-term GH replacement in adults is safe and that long-term GH replacement may even improve cardiovascular mortality and morbidity in GH-deficient adults.

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Section: Insulin Sensitivitymentioning

confidence: 85%

Safety aspects of GH replacement

Svensson¹,

Bengtsson²

2009

European Journal of Endocrinology

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“…Adults with GHD are resistant to insulin, but do not show a compensatory increase in fasting plasma insulin (31). An initial worsening in the insulin resistance with 6 weeks of rhGH therapy has been described (32). However, after 6 months of rhGH therapy, insulin levels were restored to baseline values (32), possibly as the result of the decrease in fat mass during rhGH therapy.…”

Section: Discussionmentioning

confidence: 99%

“…An initial worsening in the insulin resistance with 6 weeks of rhGH therapy has been described (32). However, after 6 months of rhGH therapy, insulin levels were restored to baseline values (32), possibly as the result of the decrease in fat mass during rhGH therapy. Therefore we think that insulin per se does not explain the differences in leptin concentration, as found in this study during rhGH therapy for 52 weeks, although a minor role cannot be excluded at this time.…”

Section: Discussionmentioning

confidence: 99%

Serum leptin levels during recombinant human GH therapy in adults with GH deficiency

Janssen¹,

Frölich

Deurenberg

et al. 1997

Eur J Endocrinol

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Objective: Recent studies suggest an involvement of the obese (ob) gene and its product leptin in the regulation of body fat. Since adults with growth hormone deficiency (GHD) have a high body fat mass which can be normalized with recombinant human (rh) GH therapy, we investigated whether GH influences serum leptin directly or indirectly via its lipolytic effect. Design: Fourteen adults with GHD were treated with subcutaneous injections of rhGH given every evening for 52 weeks. Serum leptin, fat mass and body fat percentage were measured at baseline and after 4 and 52 weeks of treatment. Methods: Serum leptin was measured with a commercially available RIA. Total body water was determined by dilution of deuterium. Fat free mass was estimated by assuming a hydration of 73%. Fat mass was estimated by subtracting fat free mass from weight. Results: At baseline, serum leptin levels were exponentially related to body fat percentage (r=0.88; P<0.0005). rhGH treatment for 4 weeks did not significantly influence serum leptin levels, whereas treatment for 52 weeks significantly decreased serum leptin levels (15.6 Ϯ 2.9 to 10.8 Ϯ 2.1 mg/l; P ¼ 0:020). Fat percentage was significantly decreased after 52 weeks of treatment (37.6 Ϯ 2.1 to 33.8 Ϯ 2.5%; P < 0:0005). The decrease in serum leptin could largely be explained by the decrease in body fat percentage, whereas the relation between leptin and body fat percentage did not change. Conclusions:The influence of GH on serum leptin is indirect, via its effect on body fat percentage. European Journal of Endocrinology 137 650-654

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“…However, BMI does not discriminate between fat and muscle mass. GH treatment in GH-deficient adults decreased body fat and increased lean body mass as determined by computed tomography and bioelectrical impedance (36). Thus increased lean body mass or altered body fat localization may mediate the observed stimulation of lipogenesis.…”

Section: Discussionmentioning

confidence: 92%

“…During longer treatments with low doses of GH, the insulin resistance is partly reversible (35,36). Higher doses, however, cause persistent insulin resistance (34) mimicking the insulin resistance of acromegaly (16).…”

Section: Discussionmentioning

confidence: 99%

Effect of growth hormone treatment on insulin action in adipocytes from children with Prader-Willi syndrome

Kamel¹,

Norgren²,

Lindgren

et al. 1998

European Journal of Endocrinology

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Objective: To study the effect of growth hormone (GH) treatment (2-4 months) on insulin action in adipocytes isolated from children with Prader-Willi syndrome (PWS), in whom GH deficiency appears to be a primary defect. We investigated the complex effects of GH on carbohydrate metabolism, as part of a current clinical trial of GH treatment in children with PWS. Methods: Biopsies of subcutaneous abdominal adipose tissue were obtained from 12 children with PWS before and after 2-4 months of GH treatment. Lipogenesis was determined by the incorporation of radiolabelled glucose into lipids in isolated adipocytes, and glycerol release to the incubation medium was used as an index of lipolysis. GLUT4 RNA was measured by solution hybridization. Results: With low glucose concentrations, at which glucose transport is rate-limiting, maximal insulininduced lipogenesis was increased by 120% after GH treatment (P < 0.05), but the sensitivity to insulin (half-maximum effective hormone concentration) was unchanged. This was not accompanied by a significant change in the RNA expression of GLUT4. Neither responsiveness (maximum effect) nor sensitivity of insulin-induced inhibition of lipolysis was affected by GH treatment. Conclusions: GH treatment of children with PWS results in an upregulation of insulin-induced lipogenesis in isolated adipocytes, with no effect on insulin-induced inhibition of lipolysis. The data suggest that the site of the effect of GH on lipogenesis is distal to the insulin hormone-receptor interaction, but does not involve altered GLUT4 expression.

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Effects of treatment with recombinant human growth hormone on insulin sensitivity and glucose metabolism in adults with growth hormone deficiency

Cited by 183 publications

References 15 publications

Safety aspects of GH replacement

Safety aspects of GH replacement

Serum leptin levels during recombinant human GH therapy in adults with GH deficiency

Effect of growth hormone treatment on insulin action in adipocytes from children with Prader-Willi syndrome

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