title: Effects of dietary weight loss on sympathetic activity and cardiac risk factors associated with the metabolic syndrome.
abstract: BACKGROUND
  Weight reduction, the first line treatment for the metabolic syndrome, improves insulin sensitivity and associated metabolic and cardiovascular abnormalities, but there is a paucity of data regarding its effect on sympathetic nervous system (SNS) activity in this clinical setting.
  
  
  OBJECTIVE
  The objectives of this study were to test the hypothesis that dietary weight loss attenuates both insulin resistance and SNS activity and to examine the relationships between SNS activity and metabolic syndrome (MetS) components.
  
  
  METHODS
  This was a single-sample, repeated measures design study.
  
  
  METHODS
  This study was performed at a tertiary referral center.
  
  
  METHODS
  Twenty-three MetS subjects (age, 58 +/- 2 yr; body mass index, 33.3 +/- 0.8 kg/m2; mean +/- sem) were studied.
  
  
  METHODS
  A hypocaloric modified Dietary Approaches to Stop Hypertension diet (26% fat, 22% protein, and 51% carbohydrate; 100 mmol/d sodium) was consumed for 3 months.
  
  
  METHODS
  The main outcome measures were postganglionic muscle sympathetic nerve activity (microneurography at a peroneal nerve), whole-body plasma norepinephrine spillover rate, spontaneous cardiac baroreflex function, and insulin sensitivity.
  
  
  RESULTS
  The hypocaloric diet significantly reduced body weight by 7% and improved all MetS components. Norepinephrine spillover decreased from 877 +/- 180 to 503 +/- 39 ng/min (P = 0.005), and muscle sympathetic nerve activity decreased from 40.6 +/- 2.1 to 34.6 +/- 2.4 bursts/min (P = 0.01), whereas cardiac baroreflex sensitivity increased by 23.0 +/- 8.0% (P = 0.02). The change in the norepinephrine spillover rate correlated positively and independently with the change in plasma leptin concentration (r = 0.49; P = 0.03).
  
  
  CONCLUSIONS
  Weight loss by a hypocaloric diet with moderate sodium restriction diminishes SNS activity in MetS subjects. This may be due to the consequences of decreased leptin concentration, enhanced insulin sensitivity, or improvements in cardiac baroreflex function.
authors.affiliation: Cardiovascular Nutrition Laboratory, Wynn Domain, Baker Heart Research Institute, P.O. Box 6492, St. Kilda Road Central, Melbourne, Victoria 8008, Australia. nora.straznicky@baker.edu.au
authors.forename: Nora E
authors.initials: NE
authors.lastname: Straznicky
authors.forename: Elisabeth A
authors.initials: EA
authors.lastname: Lambert
authors.forename: Gavin W
authors.initials: GW
authors.lastname: Lambert
authors.forename: Kazuko
authors.initials: K
authors.lastname: Masuo
authors.forename: Murray D
authors.initials: MD
authors.lastname: Esler
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Nestel
mesh_terms: D000368:Aged; D017704:Baroreflex; D002318:Cardiovascular Diseases / Q000209:etiology; D005260:Female; D006801:Humans; D007333:Insulin Resistance; D008297:Male; D024821:Metabolic Syndrome / Q000150:complications / Q000178:diet therapy* / Q000503:physiopathology; D008875:Middle Aged; D009132:Muscles / Q000294:innervation; D009638:Norepinephrine / Q000097:blood; D012307:Risk Factors; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D015431:Weight Loss
chemical_list: D009638:Norepinephrine