Aortic waveform responses to insulin in late versus early chronotype with metabolic syndrome.

Late chronotype (LC) correlates with reduced metabolic insulin sensitivity and cardiovascular disease. It is unclear if insulin action on aortic waveforms and inflammation is altered in LC versus early chronotype (EC). Adults with metabolic syndrome (n = 39, MetS) were classified as either EC (Morning-Eveningness Questionnaire [MEQ] = 63.5 ± 1.2) or LC (MEQ = 45.5 ± 1.3). A 120 min euglycemic clamp (40 mU/m(2) /min, 90 mg/dL) with indirect calorimetry was used to determine metabolic insulin sensitivity (glucose infusion rate [GIR]) and nonoxidative glucose disposal (NOGD). Aortic waveforms via applanation tonometry and inflammation by blood biochemistries were assessed at 0 and 120 min of the clamp. LC had higher fat-free mass and lower VO(2) max, GIR, and NOGD (between groups, all p ≤ 0.05) than EC. Despite no difference in 0 min waveforms, both groups had insulin-stimulated elevations in pulse pressure amplification with reduced AIx75 and augmentation pressure (AP; time effect, p ≤ 0.05). However, EC had decreased forward pressure (Pf; interaction effect, p = 0.007) with insulin versus rises in LC. Although LC had higher tumor necrosis factor-α (TNF-α; group effect, p ≤ 0.01) than EC, both LC and EC had insulin-stimulated increases in TNF-α and decreases in hs-CRP (time effect, both p ≤ 0.01). Higher MEQ scores related to greater insulin-stimulated reductions in AP (r = -0.42, p = 0.016) and Pf (r = -0.41, p = 0.02). VO(2) max correlated with insulin-mediated reductions in AIx75 (r = -0.56, p < 0.01) and AP (r = -0.49, p < 0.01). NOGD related to decreased AP (r = -0.44, p = 0.03) and Pf (r = -0.43, p = 0.04) during insulin infusion. LC was depicted by blunted forward pressure waveform responses to insulin and higher TNF-α in MetS. More work is needed to assess endothelial function across chronotypes.