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Articles by K. C Dellsperger
Total Records ( 5 ) for K. C Dellsperger
  J Yang , Y Park , H Zhang , X Xu , G. A Laine , K. C Dellsperger and C. Zhang

We hypothesized that the interaction between tumor necrosis factor- (TNF-)/nuclear factor-B (NF-B) via the activation of IKK-β may amplify one another, resulting in the evolution of vascular disease and insulin resistance associated with diabetes. To test this hypothesis, endothelium-dependent (ACh) and -independent (sodium nitroprusside) vasodilation of isolated, pressurized coronary arterioles from mLeprdb (heterozygote, normal), Leprdb (homozygote, diabetic), and Leprdb mice null for TNF- (dbTNF–/dbTNF–) were examined. Although the dilation of vessels to sodium nitroprusside was not different between Leprdb and mLeprdb mice, the dilation to ACh was reduced in Leprdb mice. The NF-B antagonist MG-132 or the IKK-β inhibitor sodium salicylate (NaSal) partially restored nitric oxide-mediated endothelium-dependent coronary arteriolar dilation in Leprdb mice, but the responses in mLeprdb mice were unaffected. The protein expression of IKK- and IKK-β were higher in Leprdb than in mLeprdb mice; the expression of IKK-β, but not the expression of IKK-, was attenuated by MG-132, the antioxidant apocynin, or the genetic deletion of TNF- in diabetic mice. Leprdb mice showed an increased insulin resistance, but NaSal improved insulin sensitivity. The protein expression of TNF- and NF-B and the protein modification of phosphorylated (p)-IKK-β and p-JNK were greater in Leprdb mice, but NaSal attenuated TNF-, NF-B, p-IKK-β, and p-JNK in Leprdb mice. The ratio of p-insulin receptor substrate (IRS)-1 at Ser307 to IRS-1 was elevated in Leprdb compared with mLeprdb mice; both NaSal and the JNK inhibitor SP-600125 reduced the p-IRS-1-to-IRS-1 ratio in Leprdb mice. MG-132 or the neutralization of TNF- reduced superoxide production in Leprdb mice. In conclusion, our results indicate that the interaction between NF-B and TNF- signaling induces the activation of IKK-β and amplifies oxidative stress, leading to endothelial dysfunction in type 2 diabetes.

  A Chockalingam , M. A Linden , M Del Rosario , G Govindarajan , K. C Dellsperger and T. R. Thomas

Hypertension, diabetes and obesity cause cardiac diastolic dysfunction (DD) which could reduce exercise capacity. Our aim was to determine if 10% weight loss by exercise at 60% VO2max five days/week (~-375 kcal/session) and caloric restriction (~-600 kcal/d) over 6 months improves exercise capacity and DD in Metabolic syndrome (MetS). Eighteen subjects (40 ± 1y, women = 6, BMI = 33.5 ± 1.0 kg/m2) successfully completed the study. Maximal treadmill stress echocardiography was performed at baseline and post weight loss to determine VO2max, resting and stress DD as the ratio of peak early diastolic mitral inflow velocity (E) to tissue Doppler early diastolic annular decent (E’). After weight loss (mean = 9.5 ± 0.2%), all metabolic parameters improved. Resting and stress E/E’ values remained normal before and after weight loss. Exercise intolerance is likely due to general deconditioning and not cardiac dysfunction in early MetS as VO2max increases significantly with lifestyle while cardiac function remains unchanged.

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