Sympathoadrenal activity in human obesity: Heterogeneity of findings since 1980

J. B. Young*, I. A. MacDonald

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

157 Scopus citations

Abstract

Alterations in sympathetic nervous system (SNS) activity are widely believed to contribute to the pathophysiology of the obese state. Disagreement, however, exists as to whether the predominant sympathetic abnormality is a decrease in neuronal activity (leading to diminished sympathetically-mediated energy expenditure and weight gain) or an increase (leading to hypertension). Findings summarized from over 40 separate studies support both hypotheses as well as the alternative thesis that SNS activity does not differ in obese humans compared to lean controls. Another abnormality being noted with increasing frequency in human obesity is reduced adrenaline (Ad) levels in plasma, both at rest or in response to a stimulus such as physical activity. Whether diminished adrenal medullary function is a cause or consequence of the obese state and whether the adrenal medulla plays any role in the regulation of energy metabolism on a daily basis are not known at the present time. Thus, while depressed SNS activity may be a sufficient explanation for the development of obesity, it is not a necessary condition. Suppressed adrenal medullary function may also contribute to this disorder.

Original languageEnglish (US)
Pages (from-to)959-967
Number of pages9
JournalInternational Journal of Obesity
Volume16
Issue number12
StatePublished - 1992

Keywords

  • Adrenal medulla
  • Epinephrine
  • Humans
  • Norepinephrine
  • Sympathetic nervous system

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Endocrinology, Diabetes and Metabolism
  • Nutrition and Dietetics

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