The Frequency of Diabetes Mellitus in Patients With Turner's Syndrome and Pure Gonadal Dysgenesis

Nielsen, J; Johansen, Klaus; Yde, Hans

doi:10.1530/acta.0.0620251

Cited by 67 publications

(16 citation statements)

References 12 publications

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“…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: 86%

“…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%

“…Although elevated fasting GH levels and lack of suppression by oral glucose were reported in patients with go nadal dysgenesis [5-8, 11, 12], no consistent abnormality in GH secretion, nor an effect of GH on carbohydrate tolerance [5,7,8], insu lin secretion or on insulin action [7,8] were observed. Moreover, in most studies the ef fects of estrogen therapy on GH secretion [22] were not considered.…”

Section: Discussionmentioning

confidence: 99%

“…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. Finally, hyperglucagonemia was noted in some patients with gonadal dysgenesis [10],…”

Section: Introductionmentioning

confidence: 98%

“…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] …”

mentioning

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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