(HealthDay News) — For women with polycystic ovary syndrome (PCOS), pancreatic beta-cell dysfunction is associated with hyperglycemia-induced nuclear factor-κB (NF-κB) activation and systemic inflammation, according to a study published in the American Journal of Physiology-Endocrinology and Metabolism.

Steven K. Malin, PhD, from the Cleveland Clinic, and colleagues examined the role of mononuclear cell (MNC)-derived inflammation in the development of beta-cell dysfunction in PCOS. 

They assessed the correlation between beta-cell function and MNC-derived NF-κB activation and tumor necrosis factor-alpha (TNF-alpha) secretion in response to an oral glucose tolerance test. The correlation was examined in normoglycemic women with PCOS (15 lean, 15 obese) and in controls (16 lean, 14 obese).

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Results indicated that, compared with lean and obese controls, there was lower first- and second-phase beta-cell function in obese women with PCOS. Women with PCOS had greater change from baseline in NF-κB activation and TNF-alpha secretion, and higher fasting thiobarbituric acid-reactive substances (TBARS), compared with lean controls. 

There was an inverse correlation for beta-cell function with NF-κB activation (first and second) and TNF-alpha-secretion (first), and with plasma TBARS and high sensitivity C-reactive protein (first and second). 

After adjustment for body fat percentage and TBARS, first- and second-phase beta-cell function remained independently linked to NF-κB activation.

“These data suggest that in PCOS, inflammation may play a role in impairing insulin secretion before the development of overt hyperglycemia,” the researchers wrote.


  1. Malin SK et al. Am J Physiol Endocrinol Metab. 2015;308(9):E770-E777.