Carbohydrate intolerance in children and adolescents with Turner syndrome

Polychronakos, Constantin; Letarte, Jacques; Collu, R.; Ducharme, J R

doi:10.1016/s0022-3476(80)80627-5

Cited by 60 publications

(46 citation statements)

References 13 publications

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“…Insulin sensitivity which, in agreement with another report (20), was already lower than in controls before starting GH treatment, decreased significantly over the first year of treatment.…”

Section: Discussionsupporting

confidence: 92%

Insulin sensitivity in Turner's syndrome: influence of GH treatment

Radetti

Pasquino²,

Gottardi³

et al. 2004

European Journal of Endocrinology

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Objective: Excessive GH secretion may lead to secondary diabetes mellitus, while prolonged GH treatment may accelerate the onset of type 2 diabetes mellitus in predisposed individuals. Turner's syndrome (TS) patients are a population at risk since they have reduced glucose tolerance (GT) spontaneously and because they are usually treated with high doses of GH. Design and methods: The aim of the study was to evaluate insulin sensitivity (IS) and glucose tolerance (GT) in a group of TS patients treated with GH for a period of 6 years. Forty-seven TS girls were included in the study. GH was administered at a mean weekly dosage of 0.35 mg/kg, injected subcutaneously over 6-7 days. GT was assessed according to the criteria of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. IS was evaluated with the quantitative insulin sensitivity check index (QUICK-I). Results: No significant increase of impaired GT was observed in the patients during the follow-up period, while a reduced IS was detected. IS in TS patients was already lower than in prepubertal controls (P , 0.001) before starting treatment and further decreased during the first year of therapy (P , 0.05), and then remained stable over the following years. No correlation was found between QUICK-I, body mass index, years of treatment, onset and duration of puberty. One patient became diabetic during the course of treatment. Conclusions: GH treatment in TS girls does not significantly increase the prevalence of impaired GT or type 2 diabetes mellitus, while it does, however, decrease IS.

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Section: Discussionsupporting

confidence: 92%

Insulin sensitivity in Turner's syndrome: influence of GH treatment

Radetti

Pasquino²,

Gottardi³

et al. 2004

European Journal of Endocrinology

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“…Since insulin resistance and carbohydrate intolerance have been reported in untreated girls with Turner’s syndrome [34, 35, 36], and supraphysiological concentrations of GH might result in insulin resistance [37, 38, 39], we investigated carbohydrate metabolism before and during GH treatment as well as after discontinuation of GH treatment. We showed that GH had no adverse effects on glucose levels, but induced higher levels of insulin (fig.…”

Section: Other Effects Of Gh Treatmentmentioning

confidence: 99%

Turner’s Syndrome: A Paediatric Perspective

Sas¹,

Keizer‐Schrama²

2001

Horm Res Paediatr

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In childhood the symptoms with the greatest impact on girls with Turner’s syndrome are: (1) congenital cardiac abnormalities (which can be corrected by surgical intervention); (2) short stature (mean adult height between 142 and 147 cm); and (3) ovarian failure (absent spontaneous puberty). Recent studies have shown that growth hormone (GH) treatment in young girls (8 years of age or younger) with Turner’s syndrome results in normalization of adult height in most of the girls when using the ‘standard’ GH dose of about 4 IU/m² per day (≈0.045 mg/kg per day). Higher GH doses (6 or 8 IU/m² per day) or the use of oxandrolone may be more effective, but their efficacy on adult height and safety in the very long term still have to be proven. If GH treatment is started early, low-dose oestrogens for induction of puberty can be given at 12 years of age without interfering with the capability of the GH treatment to normalize adult height. GH does not seem to have negative side effects on body proportions, cardiac dimensions, blood pressure, carbohydrate metabolism or bone mineral density.

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“…Impaired glucose tolerance is reported with an increased frequency in adolescents [3,4,5] and adults with TS [6, 7], with one study suggesting that insulin resistance may be the primary defect in the Turner metabolic phenotype [8]. …”

Section: Introductionmentioning

confidence: 99%

Insulin Resistance Is an Intrinsic Defect Independent of Fat Mass in Women with Turner’s Syndrome

Salgin¹,

Amin²,

Yuen³

et al. 2006

Horm Res Paediatr

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Background/Aims: Turner’s syndrome (TS) is associated with increased insulin resistance and adiposity, which might be associated with type 2 diabetes in later life. We aimed to determine whether the defect in insulin sensitivity is a primary intrinsic defect in TS or dependent on variation in body composition. Methods: Sixteen women with TS not on growth hormone replacement but receiving oestrogen replacement therapy [age (mean ± SD): 30.2 ± 8.5 years; height-corrected fat-free mass: 26.1 ± 3.1 kg/height] and a control group of 16 normal healthy women (age: 30.1 ± 8.2 years; height-corrected fat-free mass: 25.9 ± 2.4 kg/height) were studied. Fasting blood samples were obtained for measurement of glucose, insulin, IGF-I, IGFBP-1, IGFBP-3 and lipid levels. The hyperinsulinaemic euglycaemic clamp was performed to assess peripheral insulin sensitivity (M value), and the Homeostasis Model Assessment (HOMA-S) was used to estimate fasting insulin sensitivity. Body composition was assessed using a dual-energy X-ray absorptiometry scan. Results: Fasting insulin sensitivity (HOMA-S 103.2 ± 78.6 vs. 193.9 ± 93.5, p = 0.006) was lower in TS subjects compared to controls as was whole-body insulin sensitivity (M value 2.9 ± 1.9 vs. 5.5 ± 2.6 mg/kg/min, p = 0.003). In a multiple regression analysis the Turner karyotype was significantly related to insulin sensitivity (p = 0.008) independent of any differences in fat-free mass and percent whole-body fat mass. Conclusion: The increased insulin resistance in women with TS is independent of measures of body composition and may represent an intrinsic defect related to their chromosomal abnormality.

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Carbohydrate intolerance in children and adolescents with Turner syndrome

Cited by 60 publications

References 13 publications

Insulin sensitivity in Turner's syndrome: influence of GH treatment

Insulin sensitivity in Turner's syndrome: influence of GH treatment

Turner’s Syndrome: A Paediatric Perspective

Insulin Resistance Is an Intrinsic Defect Independent of Fat Mass in Women with Turner’s Syndrome

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