Growth hormone-deficient adults are insulin-resistant

Johansson, Jan‐Ove; Fowelin, J.; Landin, Kerstin; Lager, I; Bengtsson, Bengt‐Åke

doi:10.1016/0026-0495(95)90004-7

Cited by 261 publications

(176 citation statements)

References 28 publications

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“…The latter results and results of in vitro studies in both human and rodent fat cells (30) suggest that insulin may play some role in leptin production. 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).…”

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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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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“…On the other hand, patients with growth hormone deficiency also have visceral obesity and an increased insulin resistance even when correcting for body fat (63). Thus, both an excess of, and a deficiency in GH can result in insulin resistance.…”

Section: Other Neuroendocrine Pathwaysmentioning

confidence: 99%

Neuroendocrine mechanisms in insulin resistance

Sjöstrand

Eriksson

2009

Molecular and Cellular Endocrinology

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Dysregulated hormonal, metabolic and neural signalling within and between organs can contribute to development of metabolic diseases including type 2 diabetes. Insulinantagonistic effects of hormones, cytokines and excess metabolic substrates such as glucose and fatty acids may be exerted via common mechanisms involving for example reactive oxygen species (ROS) accumulation and associated inflammatory responses.Visceral adiposity is a central component of the metabolic syndrome and it is also strongly associated with insulin resistance. Both visceral obesity and insulin resistance are important risk factors for the development of type 2 diabetes. In the development of insulin resistance, it is likely that intra-abdominal adipose tissue plays a critical role in a complex endocrine and neural network involving several tissues. This review paper focuses on neuroendocrine 'stress' factors that target insulin-responsive tissues, in particular adipose tissue. We propose that there are common pathways by which dysregulation in different endocrine systems may contribute to the development of type 2 diabetes.

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“…Indeed, untreated GH deficiency (GHD) in adult life is associated with abnormalities in body composition in addition to other cardiovascular risk factors, such as altered cardiac structure and function, dyslipidemia, glucose intolerance and insulin resistance and GH treatment (GHT) exerts beneficial effects on most of these alterations [3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

The visceral adiposity index is associated with insulin sensitivity and IGF-I levels in adults with growth hormone deficiency

2016

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The visceral adiposity index, based on anthropometric and metabolic parameters, has been shown to be related to adipose tissue function and insulin sensitivity. We aimed to evaluate the performance of the visceral adiposity index in adult patients with growth hormone deficiency. We enrolled 52 patients(mean age 51 ± 13 years) with newly diagnosed growth hormone deficiency and 50 matched healthy subjects as controls at baseline. At baseline and after 12 and 24 months of treatment we evaluated anthropometric measures, lipid profile, glucose and insulin during an oral glucose tolerance test, hemoglobin A1c, homeostasis model assessment estimate of insulin resistance, quantitative insulin sensitivity check index, insulin sensitivity index Matsuda, insulin-like growth factor-I and visceral adiposity index. At baseline growth hormone deficiency patients showed higher waist circumference (p < 0.001), low-density lipoprotein cholesterol (p < 0.001) and visceral adiposity index (p = 0.003) with lower insulin sensitivity index (p = 0.007) and high-density lipoprotein cholesterol (p = 0.001) than controls. During growth hormone treatment we observed a significant increase in insulin-like growth factor-I (p < 0.001), high-density lipoprotein (p < 0.001) with a trend toward increase in insulin sensitivity index (p = 0.055) and a significant decrease in total cholesterol (p < 0.001) and visceral adiposity index (p < 0.001), while no significant changes were observed in other clinical and metabolic parameters. The visceral adiposity index was the only parameter that significantly correlated with growth hormone peak at diagnosis (p < 0.001) and with insulin-like growth factor-I and insulin sensitivity index both at diagnosis (p = 0.009 and p < 0.001) and after 12 (p = 0.026 and p = 0.001) and 24 months (p < 0.001 and p = 0.001) of treatment. The visceral adiposity index, which has shown to be associated with both insulin-like growth factor-I and insulin sensitivity, proved to be the most reliable index of metabolic perturbation, among the most common indexes of adiposity assessment and a marker of benefit during treatment in adult growth hormone deficiency patients.

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Growth hormone-deficient adults are insulin-resistant

Cited by 261 publications

References 28 publications

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

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

Neuroendocrine mechanisms in insulin resistance

The visceral adiposity index is associated with insulin sensitivity and IGF-I levels in adults with growth hormone deficiency

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