title: Leptin and heart sympathetic activity in normotensive obese and non-obese subjects.
abstract: BACKGROUND
  In rats leptin increases sympathetic activity, and an inhibitory effect on leptin synthesis and release has been demonstrated for the catecholamines, both in adipocyte cell cultures and in healthy experimental animals. The aim of this study was to evaluate the relationship between leptin and heart sympathetic activity as well as changes in leptin levels after the administration of drugs that modify sympathetic activity.
  
  
  METHODS
  We performed a randomized, blinded, before-after trial in 81 normotensive obese and non-obese subjects. They were studied before and after treatment with enalapril (5 mg every 12 hours) or clonidine (0.1 mg every 12 hours) for 7 days.
  
  
  RESULTS
  Obese subjects had higher values for percent body fat (p < 0.0005), triglycerides (p < 0.05), leptin (p < 0.0005), and low frequency/high frequency ratio at night (LF/HFn, p = 0.05). After enalapril or clonidine treatment, leptin levels were not modified. Both drugs significantly diminished the systolic and diastolic blood pressures. In the obese group, clonidine and enalapril diminished the LF/HFn ratio (p < 0.05). The LF/HF index showed a univariate correlation with body mass index, leptin, systolic blood pressure, insulin, age and triglyceride levels. In the multiple regression analysis for factors associated with the LF/HF ratio, only leptin, age and insulin were included in the model. The r2 of the model was 0.3 (p = 0.0003).
  
  
  CONCLUSIONS
  A higher level of heart sympathetic activity is found in normotensive obese as compared with non-obese subjects. Both clonidine and enalapril reduced heart sympathetic activity in obese subjects without a change in fasting leptin levels.
authors.affiliation: Epidemiology Research Unit, Mexican Institute of Social Security, León.
authors.forename: Norma
authors.initials: N
authors.lastname: Amador
authors.forename: Elva
authors.initials: E
authors.lastname: Pérez-Luque
authors.forename: Juan Manuel
authors.initials: JM
authors.lastname: Malacara
authors.forename: Juan Manuel
authors.initials: JM
authors.lastname: Guízar
authors.forename: Ramon
authors.initials: R
authors.lastname: Paniagua
authors.forename: Susano
authors.initials: S
authors.lastname: Lara
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism; D000316:Adrenergic alpha-Agonists / Q000008:administration & dosage; D000328:Adult; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage; D000959:Antihypertensive Agents / Q000008:administration & dosage; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects; D015992:Body Mass Index; D003000:Clonidine / Q000008:administration & dosage; D003971:Diastole / Q000187:drug effects; D004656:Enalapril / Q000008:administration & dosage; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology*; D020738:Leptin / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology*; D013223:Statistics as Topic; D013599:Systole / Q000187:drug effects; D016896:Treatment Outcome
chemical_list: D000316:Adrenergic alpha-Agonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D015415:Biomarkers; D020738:Leptin; D004656:Enalapril; D003000:Clonidine