Decreased peripheral insulin sensitivity in hyperprolactinemic patients

Luger, Anton; H, Graf; Prager, Rudolf; Schernthaner, Gerit-Holger

doi:10.1530/acta.0.107s044

Cited by 4 publications

(6 citation statements)

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“…glucose administration. The discrepancy between the report of Hagen et al 15 ) and the other reports including the present study 10 – 14 ) could be due to the transient and less pronounced hyperprolactinemia induced in the normal men in his study. Whereas, we and other investigators studied women with pituitary tumors.…”

Section: Discussioncontrasting

confidence: 86%

“…Schernthaner et al 11 ) reported that hyperprolactinemic women had impaired insulin receptor binding in vitro, which might decrease insulin effectiveness in vivo. The existence of in vivo insulin resistance in severe hyperprolactinemia was also supported by the findings obtained in hyperglycemic clamp study showing diminished peripheral insulin sensitivity 14 ) .…”

Section: Discussionmentioning

confidence: 63%

“…The underlying mechanism of hyperinsulinemia in women with chronic prolactin excess was not pursued in the present study. Various experimental and clinical studies suggest that severe hyperprolactinemia is associated with a diminished sensitivity of peripheral tissue to insulin 9 – 11 , 14 ) . In fact, our findings of hyperinsulinemia in the presence of mild glucose intolerance reflect insulin resistance.…”

Section: Discussionmentioning

confidence: 99%

“…It has been suggested that prolactin is a diabetogenic hormone 9 ) . Various clinical studies in hyperprolactinemic women with or without pituitary tumors have revealed insulin resistance and hyperinsulinemia 10 – 14 ) . In these studies, impaired glucose tolerance was noted in some but not all women.…”

Section: Introductionmentioning

confidence: 99%

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Direct Relationship between Elevated Free Testosterone and Insulin Resistance in Hyperprolactinemic Women

Kim

Sung

et al. 1993

Korean J Intern Med

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Women with hyperprolactinemia have been reported to have hyperandrogenemia and/or insulin resistance. However, little is known about the association of hyperandrogenemia and insulin resistance in these women. To investigate whether hyperandrogenemia and/or insulin resistance occur in hyperprolactinemic women, and to assess the relationship between them, we measured basal androgen level and both glucose and insulin levels after oral glucose administration in 20 hyperprolactinemic women and 7 female control subjects. Free testosterone level was higher and estradiol level lower in hyperprolactinemic women than in control subjects (p<0.05), whereas dehydroepiandrosterone sulfate (DHEAS) and total testosterone levels were similar (p>0.05). Both fasting glucose and insulin levels didn’t differ in the two groups (p>0.05). However, both serum glucose and insulin levels, after a 75 g glucose load, were significantly increased in hyperprolactinemic women (p=0.001, p <0.001, respectively). In simple linear regression analysis in hyperprolactinemic women, only free testosterone level had a positive correlation with the incremental area under the insulin curve (insulin-IAU) (r=0.47, p<0.05). In multiple stepwise regression analysis, free testosterone level, mean blood pressure and DHEAS level were associated significantly with insulin-IAU (beta=0.98, p<0.0001; beta=0.58, p=0.002; beta=−0.67, p=0.003, respectively) These results suggest that insulin resistance is closely related to elevated free testosterone level in hyperprolactinemic women.

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Section: Discussioncontrasting

confidence: 86%

Section: Discussionmentioning

confidence: 63%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Direct Relationship between Elevated Free Testosterone and Insulin Resistance in Hyperprolactinemic Women

Kim

Sung

et al. 1993

Korean J Intern Med

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“…This peculiar plasma glucose pattern could be due to the well-known insulin resistance present in obesity (4). The evidence that hyperprolactinemic patients showed an ARG-induced glucose pattern similar to normals suggests that insulin hypersécrétion is not due to peripheral insulin resistence (10,30).…”

Section: Discussionmentioning

confidence: 99%

Effects of glucose load and/or arginine on insulin and growth hormone secretion in hyperprolactinemia and obesity

Maccario

Grottoli²,

Razzore³

et al. 1996

European Journal of Endocrinology

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In hyperprolactinemic patients an exaggerated glucose-induced insulin secretion has been reported, but these results have not been confirmed by other researchers. On the other hand, there are few data concerning somatotrope secretion in this condition. In order to clarify these points, in seven normal weight hyperprolactinemic female patients (HP: age 18-46 years, body mass index = 21.8 +/- 0.6 kg/m(2), basal prolactin = 91.7 +/- 16.5 micrograms/l) we studied the effects of glucose load (100 g orally) and/or arginine (0.5 g/kg infused over 30 min) on insulin glucose and growth hormone (GH) levels. These results were compared with those obtained in seven patients with simple obesity (OB: age 23-48 years, body mass index = 38.3 +/- 2.6 kg/m(2)) in whom exaggerated insulin and low GH secretion are well known. Seven normal women (NS: age 26-32 years, body mass index = 20.6 +/- 1/9 kg/m(2)) were studied as controls. The insulin response to glucose in HP (area under curve = 11,460.8 +/- 1407.5 mU x min x l(-1)) was not significantly different from NS (7743.7 +/- 882.9 mU x min x l(-1)) and OB (14,504.8 +/- 1659.9 mU x min x l(-1)). The arginine-induced insulin release in HP and OB was similar (4219.4 +/- 631.7 and 4107.3 +/- 643.2 mU x min x l(-1), respectively), both being higher (p < 0.02) than in NS (2178.1 +/- 290.9 mU x min x l(-1). Glucose and arginine had an additive effect on insulin release in HP and NS (19,769.1 +/- 3249.6 and 10,996.6 +/- 1201.0 mU x min 1(-1), respectively) and a synergistic effect in OB (28 117.3 +/- 5224.7 mU x min x l(-1)). In HP the insulin response to the combined administration of glucose and arginine was not significantly different from the one in OB, and both were higher (p < 0.05) than in NS. The increase in glucose levels after glucose administered on its own or combined with arginine was higher (p < 0.02) and longer lasting in OB than in NS and HP. After arginine in OB, the glucose levels did not show the late decrease under baseline values observed in HP and NS. Glucose inhibited GH secretion both in HP and NS (p < 0.05), while arginine stimulated it in all groups, although the GH response in HP and NS was higher (p < 0.03) than in OB. The arginine-induced GH secretion was inhibited by glucose in HP and NS but not in OB. These results demonstrate that both in hyperprolactinemic patients and in obesity there is a clear increase in insulin secretion. The insulin hyperresponsiveness in hyperprolactinemia is more clearly demonstrated by combined stimulation with glucose and arginine. In spite of similar insulin hypersecretion in hyperprolactinemic and obese patients, GH secretion is reduced only in the latter; with these data the hypothesis that somatotrope insufficiency in obesity is due to hyperinsulinism is unlikely.

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Theoretische Erklärungsansätze zur Ableitung von Gestaltungsaussagen für das Preismanagement im Einzelhandel

Preismanagement Im Einzelhandel

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Decreased peripheral insulin sensitivity in hyperprolactinemic patients

Cited by 4 publications

References 0 publications

Direct Relationship between Elevated Free Testosterone and Insulin Resistance in Hyperprolactinemic Women

Direct Relationship between Elevated Free Testosterone and Insulin Resistance in Hyperprolactinemic Women

Effects of glucose load and/or arginine on insulin and growth hormone secretion in hyperprolactinemia and obesity

Theoretische Erklärungsansätze zur Ableitung von Gestaltungsaussagen für das Preismanagement im Einzelhandel

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