Glucose Tolerance Tests and Insulin Response in Juvenile Patients with Gonadal Dysgenesis

Karp, M; Snir, Adaya Weissler; Doron, M.; Mammon, Zipora; Laron, Zvi

doi:10.1159/000400802

Cited by 6 publications

(9 citation statements)

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“…The incidence of impaired glucose tolerance in 43% of our patients is similar to the reports of some [4,6], but greater than that found by others in similar age group patients [3].…”

Section: Discussionsupporting

confidence: 91%

“…In con trast with the reports of other investigators who noted diminished insulin secretion [6][7][8][9]11] in patients with gonadal dysgenesis, we, and others found normal [5] or increased [2,3,5,10] insulin responses to beta cell secretagogues. The discrepancy between our find ings and the contrary observations reported by others is unclear.…”

Section: Discussionsupporting

confidence: 85%

“…Several reasons have been suggested to explain the abnormal carbohydrate metabo lism in gonadal dysgenesis, including genetic [1,2], excess GH secretion [12], estrogen treatment [3], diminished insulin secretion [6][7][8][9]11] and insulin resistance [5]. In con trast with the reports of other investigators who noted diminished insulin secretion [6][7][8][9]11] in patients with gonadal dysgenesis, we, and others found normal [5] or increased [2,3,5,10] insulin responses to beta cell secretagogues.…”

Section: Discussionsupporting

confidence: 69%

“…Disturbances in insulin and growth hormone (GH) secretions, and factors such as family history of diabetes [1], estro gen therapy [6] and age have been implicated. In patients with glucose intolerance, subnor mal insulin responses to oral glucose and intravenous tolbutamide were noted in some studies [6][7][8][9], while others found normal [5] or higher than normal insulin levels [2,3,6,10] in response to these stimuli. Others have found diminished [11] and higher than nor mal [2,3] insulin responses to glucose in patients with normal glucose tolerance.…”

Section: Introductionmentioning

confidence: 99%

“…In patients with glucose intolerance, subnor mal insulin responses to oral glucose and intravenous tolbutamide were noted in some studies [6][7][8][9], while others found normal [5] or higher than normal insulin levels [2,3,6,10] in response to these stimuli. Others have found diminished [11] and higher than nor mal [2,3] insulin responses to glucose in patients with normal glucose tolerance. Al though elevated GH levels and a paradoxical rise in GH with hyperglycemia were ob served in patients with gonadal dysgenesis [5,7,8,11,12], no clear relationship of GH to glucose intolerance was found.…”

Section: Introductionmentioning

confidence: 99%

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Carbohydrate Intolerance in Gonadal Dysgenesis: Evidence for Insulin Resistance and Hyperglucagonemia

Costin¹,

Kogut²

1985

Horm Res

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To determine the pathogenesis of carbohydrate intolerance associated with gonadal dysgenesis, plasma glucose, insulin, glucagon, and growth hormone responses to oral glucose and intravenous tolbutamide, arginine and insulin were evaluated in 21 nonobese patients, 7–19 years old. Glucose intolerance was present in 9 of 21 nonobese patients (42.8%). Insulin levels, the area under the insulin curve after oral glucose and intravenous tolbutamide and the insulin to glucose ratio were significantly greater in patients than in controls (p < 0.005). The decrease in plasma glucose following intravenous tolbutamide was significantly less in patients than in controls (p < 0.05) despite insulin levels which were greater than in controls (p < 0.05). After intravenous insulin, plasma glucose fell significantly less in patients than in controls (p < 0.01). Plasma glucagon levels and the area under the glucagon curve after oral glucose and arginine infusion were significantly greater in patients than in controls (p < 0.005 and p < 0.01, respectively). The increase in glucagon after insulin-induced hypoglycemia was significantly less in patients than in controls (p < 0.025). Fasting and stimulated growth hormone levels and the mean 24-hour growth hormone concentration were similar in patients and controls. These results indicate that glucose intolerance occurs frequently in gonadal dysgenesis and is associated with normal or increased insulin secretory responses. These abnormalities are probably due to insulin resistance and hyperglucagonemia. The decrease in insulin action does not appear to result from excessive growth hormone secretion or treatment with anabolic steroids or estrogen-progesterone medications.

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“…The incidence of impaired glucose tolerance in 43% of our patients is similar to the reports of some [4,6], but greater than that found by others in similar age group patients [3].…”

Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 85%

Section: Discussionsupporting

confidence: 69%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Carbohydrate Intolerance in Gonadal Dysgenesis: Evidence for Insulin Resistance and Hyperglucagonemia

Costin¹,

Kogut²

1985

Horm Res

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The abnormalities of carbohydrate metabolism in Turner syndrome: analysis of risk factors associated with impaired glucose tolerance

Choi

Kim

2005

Eur J Pediatr

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A Comparative Study of the Effect of Oestrogen Substitution Therapy on Breast Development in Girls With Hypo—and Hypergonadotrophic Hypogonadism

Pertzelan

Yalon

Kauli

et al. 1982

Clinical Endocrinology

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During treatment of girls with oestrogen deficiency we observed different patterns of breast development in response to therapy. The forty-five girls studied fell into four groups: Group A, gonadal dysgenesis; Group B, isolated gonadotrophin deficiency; Group C, multiple pituitary hormone deficiencies; Group D, congenital adrenal hyperplasia (17-alpha-hydroxylase deficiency). Treatment with oestrogen was given in an identical manner to all. In the patients with gonadal dysgenesis, in whom the hypothalamic-pituitary function was normal, treatment led to full breast development. In isolated gonadotrophin deficiency and multiple pituitary hormone deficiency breast development was incomplete even after 3 years or more of oestrogen treatment. The conspicuous difference in the hormonal status is that the latter two groups lack gonadotrophins, while in gonadal dysgenesis these hormones are grossly elevated. Our conclusion is that gonadotrophins play an important role in mammary gland development, a finding not previously described. In the girl with 17-alpha-hydroxylase deficiency we observed that cortisol was necessary, in addition to sex hormones, for normal breast development.

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Glucose Tolerance Tests and Insulin Response in Juvenile Patients with Gonadal Dysgenesis

Cited by 6 publications

References 0 publications

Carbohydrate Intolerance in Gonadal Dysgenesis: Evidence for Insulin Resistance and Hyperglucagonemia

Carbohydrate Intolerance in Gonadal Dysgenesis: Evidence for Insulin Resistance and Hyperglucagonemia

The abnormalities of carbohydrate metabolism in Turner syndrome: analysis of risk factors associated with impaired glucose tolerance

A Comparative Study of the Effect of Oestrogen Substitution Therapy on Breast Development in Girls With Hypo—and Hypergonadotrophic Hypogonadism

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