Hyperinsulinemia Potentiates Airway Responsiveness to Parasympathetic Nerve Stimulation in Obese Rats

• DOI: 10.1165/rcmb.2013-0452oc
• Publication Date: 2014-03-07T15:51:53Z
• Authors: Zhenying Nie; David B. Jacoby; Allison D. Fryer
• Keywords: Hyperinsulinemia

Obesity is a substantial risk factor for developing asthma, but the molecular mechanisms underlying this relationship are unclear. We tested role of insulin in airway responsiveness to nerve stimulation using rats genetically prone or resistant diet-induced obesity. Airway response vagus and M2 M3 muscarinic receptor function were measured obese-prone -resistant with high low circulating insulin. The effects on nerve-mediated human smooth muscle contraction vitro. Our data show that increased vagally mediated bronchoconstriction obesity associated hyperinsulinemia loss inhibitory parasympathetic nerves. did not induce inflammation increase wall thickness. Smooth acetylcholine was increased, indicating hyperresponsiveness at level Reducing serum streptozotocin protected neuronal prevented obese rats. Replacing restored dysfunction receptors streptozotocin-treated Treatment caused function, resulting obese-resistant rats, inhibited This study shows it per se accompanying potentiates induced by inhibiting increasing release from