Response to Comment on: Straznicky et al. Neuroadrenergic Dysfunction Along the Diabetes Continuum: A Comparative Study in Obese Metabolic Syndrome Subjects. Diabetes 2012;61:2506–2516

  1. Gavin W. Lambert
  1. From the Human Neurotransmitters Laboratory, Baker IDI Heart & Diabetes Institute, Melbourne, Victoria, Australia
  1. Corresponding author: Nora E. Straznicky, nora.straznicky{at}bakeridi.edu.au.

We wish to thank Dr. Frontoni (1) for her insightful comments regarding the disparate relationship of glucose utilization to two indices of sympathetic nervous system activity—whole-body norepinephrine spillover rate and muscle sympathetic nerve activity (MSNA), within our cohort of obese metabolic syndrome subjects (2). Both arterial norepinephrine concentration and norepinephrine spillover rate showed a strong inverse relationship with clamp-derived glucose utilization (M/I value, r = −0.47, P = 0.008), whereas MSNA was not significantly associated with glucose utilization. Rather, total MSNA was influenced by the prevailing insulin concentration as indicated by positive associations with fasting C-peptide levels (r = 0.37, P = 0.04) and insulin area under the curve …

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