Adiponectin and resistin serum levels in women with polycystic ovary syndrome during oral glucose tolerance test: A significant reciprocal correlation between adiponectin and resistin independent of insulin resistance indices
UNSPECIFIED (2005) Adiponectin and resistin serum levels in women with polycystic ovary syndrome during oral glucose tolerance test: A significant reciprocal correlation between adiponectin and resistin independent of insulin resistance indices. MOLECULAR GENETICS AND METABOLISM, 85 (1). pp. 61-69. ISSN 1096-7192Full text not available from this repository.
Polycystic ovary syndrome (PCOS) is associated with an increased incidence of insulin resistance (IR), obesity, and type 2 diabetes. Resistin, an adipocytokine, may represent a link between obesity, and these metabolic disorders. There is also evidence that inflammation is a hyperresistinemic state in humans, and cytokine induction of resistin may contribute to insulin resistance in endotoxemia, obesity, and other inflammatory states. In contrast, adiponectin, increases insulin sensitivity, improves glucose tolerance, inhibits inflammatory pathways, while adenovirus-expressed adiponectin reduces atherosclerotic lesions in a mouse model of atherosclerosis. We aimed to assess, in women with PCOS, whether there is a relationship between adiponectin and resistin and the indices of IR, and whether serum levels of these adipocytokines are altered by glucose-induced hyperinsulinaemia. Serum levels of resistin and adiponectin were measured at 0, 60, and 120 min during 75 g oral glucose tolerance test (OGTT), in 19 women with PCOS, age 36.3 +/- 11.4 years (mean +/- SD), body mass index (BMI) 29.3 +/- 7.7 kg/m(2), and correlated with the indices of IR, such as HOMA-IR, QUICKI, and the insulin resistance index calculated from glucose and insulin levels obtained during OGTT. There was no change in resistin concentrations (7.31 +/- 4.58, 7.47 +/- 5.40, 7.22 +/- 5.12 pg/ml, at 0, 60, and 120 min of OGTT, respectively, P = 0.77), but there was an increase in adiponectin from 11.32 +/- 4.64 mu g/ml at baseline to 14.78 +/- 7.41 gg/ml, at 120 min of OGTT (P < 0.01). The magnitude of the overall rise in adiponectin was greater from 60 to 120 min (from 12.31 +/- 5.72 to 14.78 +/- 7.41 mu g/ml, P < 0.006). Neither resistin, nor adiponectin correlated with the indices of IR, lipids, or other hormonal parameters of the PCOS. There was, however, a significant negative correlation between serum resistin and adiponectin (P = 0.001). In conclusion, we observed a strong negative correlation between serum adiponectin and resistin, despite the lack of direct correlation with the indices of IR. Given the opposite effects of resistin and adiponectin on the inflammatory process, we speculate that relative proportion of adiponectin-to-resistin might potentially influence cardiometabolic risk in women with the PCOS independently of IR parameters. The observed increase in adiponectin during OGTT requires further study. (c) 2005 Elsevier Inc. All rights reserved.
|Item Type:||Journal Article|
|Subjects:||Q Science > QD Chemistry
Q Science > QH Natural history > QH426 Genetics
|Journal or Publication Title:||MOLECULAR GENETICS AND METABOLISM|
|Publisher:||ACADEMIC PRESS INC ELSEVIER SCIENCE|
|Number of Pages:||9|
|Page Range:||pp. 61-69|
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