(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).
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.