title: Higher heart rate may predispose to obesity and diabetes mellitus: 20-year prospective study in a general population.
abstract: BACKGROUND
  Emerging evidence indicates an association between sympathetic activation and metabolic syndrome. However, sympathetic activation in metabolic syndrome may be a cause, consequence, or just epiphenomenon. To elucidate this issue, the predictive power of resting heart rate for the development of abnormal glucose and lipid metabolisms after 20 years was evaluated in a general population.
  
  
  METHODS
  A total of 637 participants (>20 years old) underwent a health examination in 1979 including measurements of blood chemistries. Resting heart rate (bpm) was measured by an electrocardiogram. In 1999, all of the study participants again underwent a health examination, including electrocardiogram and blood chemistries. Because four of them had atrial fibrillation, and 19 subjects were taking antihypertensive medication in 1979, they were excluded from analysis. Therefore, a complete dataset of 614 subjects was available.
  
  
  RESULTS
  As was reported in our previous article, in 1999 we found a linear and significant (P < 0.05) cross-sectional relationship between resting heart rate and a cluster of cardiometabolic risk factors (blood pressure (BP), free fatty acid (FFA), plasma glucose, and homeostasis model assessment (HOMA) index). Baseline higher heart rate (heart rate >or=80 bpm in 1979) predicted the development of obesity, diabetes mellitus (DM), and insulin resistance in 1999 after adjustments for age, sex, and other confounders.
  
  
  CONCLUSIONS
  This is one of the first prospective reports demonstrating that higher heart rate may predispose to the development of obesity and DM, suggesting that the sympathetic nerve system may play a role in the development of obesity and DM.
authors.affiliation: Department of Internal Medicine, Division of Cardio-Vascular Medicine, Kurume University School of Medicine, Kurume, Japan.
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Shigetoh
authors.forename: Hisashi
authors.initials: H
authors.lastname: Adachi
authors.forename: Sho-ichi
authors.initials: S
authors.lastname: Yamagishi
authors.forename: Mika
authors.initials: M
authors.lastname: Enomoto
authors.forename: Ako
authors.initials: A
authors.lastname: Fukami
authors.forename: Maki
authors.initials: M
authors.lastname: Otsuka
authors.forename: Shun-ichi
authors.initials: S
authors.lastname: Kumagae
authors.forename: Kumiko
authors.initials: K
authors.lastname: Furuki
authors.forename: Yasuki
authors.initials: Y
authors.lastname: Nanjo
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Imaizumi
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects* / Q000502:physiology; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D003920:Diabetes Mellitus / Q000209:etiology*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D007564:Japan; D008297:Male; D024821:Metabolic Syndrome / Q000209:etiology; D008875:Middle Aged; D009765:Obesity / Q000209:etiology*; D011446:Prospective Studies
chemical_list: D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified