Obese reproductive-age @entity1 exhibit a proatherogenic inflammatory response during XXXX .

@entity1 @entity650 @entity32 @entity2451 @entity28 @entity1356 @entity26 @entity4854 @entity413
OBJECTIVE: The objective was to determine if physiological @entity4854 induces a proatherogenic inflammatory response in mononuclear cells (MNCs) in @entity28 reproductive-age @entity1 . RESEARCH METHODS AND PROCEDURES: Seven @entity28 and 6 age-matched lean @entity1 (20 to 39 years of age) underwent a 2-hour 75-g oral @entity413 tolerance test. The release of @entity650 ( @entity650 ) and @entity1356 ( @entity1356 ) from MNCs cultured in the presence of lipopolysaccharide (LPS) was measured after isolation from blood samples drawn fasting and 2 hours after @entity413 ingestion. Reactive @entity26 species (ROS) generation and intra-nuclear nuclear factor kappaB ( @entity2451 ) from MNCs were quantified from the same blood samples. Insulin resistance was estimated by homeostasis model assessment of insulin resistance (HOMA-IR). Total body fat and truncal fat were determined by DXA. RESULTS: Obese @entity1 had a higher (p < 0.03) total body fat (42.2 +/- 1.1 vs. 27.7 +/- 2.0%), truncal fat (42.1 +/- 1.2 vs. 22.3 +/- 2.4%), and HOMA-IR (3.3 +/- 0.5 vs. 1.8 +/- 0.2). LPS-stimulated @entity650 release from MNCs was suppressed during @entity4854 in lean subjects (1884 +/- 495 vs. 638 +/- 435 pg/mL, p < 0.05) but not in @entity28 @entity1 (1184 +/- 387 vs. 1403 +/- 498 pg/mL). There was a difference (p < 0.05) between groups in the @entity4854 -induced MNC-mediated release of @entity650 (-1196 +/- 475 vs. 219 +/- 175 pg/mL) and @entity1356 (-79 +/- 43 vs. 17 +/- 12 pg/mL). In addition, the @entity28 group exhibited increased (p < 0.05) MNC-derived ROS generation (39.3 +/- 9.9 vs. -1.0 +/- 12.8%) and intra-nuclear @entity2451 (9.4 +/- 7.3 vs. -23.5 +/- 13.5%). Truncal fat was positively correlated with the MNC-derived @entity650 response (rho = 0.58, p < 0.05) and intra-nuclear @entity2451 (rho = 0.64, p < 0.05). DISCUSSION: These data suggest that @entity28 reproductive-age @entity1 are unable to suppress proatherogenic @entity32 during physiological @entity4854 . Increased adiposity may be a significant contributor to this pro-inflammatory susceptibility.
