Relation of obesity and diet to sympathetic nervous system activity

Rebecca J. Troisi, Scott T. Weiss*, Donna R. Parker, David Sparrow, James B. Young, Lewis Landsberg

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

228 Scopus citations


The hypothesis that dietary intake and obesity stimulate the sympathetic nervous system was investigated in a cross-sectional study of 572 men aged 43-85 years from the Normative Aging Study. Habitus was represented by body mass index, as a measure of overall adiposity, and by the ratio of abdomen-to-hip circumference (abdomen/hip ratio), as a measure of centripetal fat distribution. Sympathetic activity was assessed by measurement of 24-hour urinary norepinephrine excretion. Increased body mass index and total caloric intake were independently associated with increased 24-hour urinary norepinephrine excretion (p=0.0001 and p=0.0055, respectively). In addition, mean urinary norepinephrine excretion was higher in subjects classified as either hyperglycemic (serum fasting glucose ≥113 mg/dl) and hyperinsulinemic (serum fasting insulin ≥19 μuIU/ml) (p=0.0023) or in subjects classified as either hyperglycemic or hyperinsulinemic (p=0.0063) than the mean urinary norepinephrine excretion in normal subjects. These relations were demonstrated to be independent of age, smoking status, and physical activity. Our results are consistent with the hypothesis that insulin mediates sympathetic stimulation in response to dietary intake and increases sympathetic nervous system activity in the obese.

Original languageEnglish (US)
Pages (from-to)669-677
Number of pages9
Issue number5
StatePublished - May 1991


  • Body fat distribution
  • Diet
  • Epinephrine
  • Norepinephrine
  • Obesity
  • Sympathetic nervous system

ASJC Scopus subject areas

  • Internal Medicine


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