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DOI 10.1055/s-0029-1210675

Медицинская библиотека · Experimental and clinical endocrinology · 1987

Pancreatic beta cell function in polycystic ovary syndrome: its relationship to body weight, serum testosterone and serum prolactin levels.

Prelević G M, Würzburger M I, Perić L A

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Аннотация

Circulating levels of insulin and C-peptide in response to oral glucose administration (75 g) were measured in 25 PCOS patients (13 were obese and 12 non-obese) without acanthosis nigricans and in 12 non-obese normal cycling women of similar age. Fasting levels of insulin and C-peptide as well as the sums of their levels in response to glucose were significantly greater in PCO patients than in controls despite similar glucose responses. Obese PCO patients had greater basal levels, maximum increments and sums of insulin and C-peptide levels than non-obese PCO patients and controls. PCO patients with increased basal total testosterone levels had significantly greater mean fasting insulin levels (p less than 0.005) than those with normal testosterone levels but their responses to glucose were not significantly different. Hyperprolactinaemic PCO patients had neither basal level nor sums of insulin and C-peptide levels in response to glucose greater than normoprolactinaemic PCO patients. In all PCO patients BMI correlated significantly with insulin (p less than 0.05) and C-peptide levels (p less than 0.001). Total serum testosterone levels correlated significantly with fasting levels and the sum of C-peptide levels in response to glucose. The correlations of total serum testosterone levels with fasting and the sum of insulin levels in response to glucose were also positive but not significant. These results clearly indicate that in PCOS there is a significant degree of hyperinsulinaemia which is mainly related to obesity.

Для цитирования: Prelević G M, Würzburger M I, Perić L A. Pancreatic beta cell function in polycystic ovary syndrome: its relationship to body weight, serum testosterone and serum prolactin levels.. Experimental and clinical endocrinology. 1987. DOI: 10.1055/s-0029-1210675.

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