title: Blunted lipolytic response to fasting in abdominally obese women: evidence for involvement of hyposomatotropism.
abstract: BACKGROUND
  Abdominal obesity is associated with a blunted lipolytic response to fasting that may contribute to the preservation of adipose tissue mass.
  
  
  OBJECTIVE
  To further explore the pathophysiology of blunted lipolysis during fasting in obesity, we simultaneously measured lipolysis and distinct neuroendocrine regulatory hormones in abdominally obese and normal-weight (NW) women.
  
  
  METHODS
  Eight abdominally obese [x +/- SD body mass index (BMI; in kg/m(2)): 32.1 +/- 2.6] and 6 NW (BMI: 22.7 +/- 1.5) women were studied during the last 8 h of a 20-h fast. The glycerol appearance rate and the serum and plasma concentrations of insulin, leptin, cortisol, and growth hormone were measured regularly.
  
  
  RESULTS
  At 13 h of fasting, the mean (+/-SD) glycerol appearance rate corrected for fat mass was greater in NW women than in obese women (7.2 +/- 1.0 and 5.1 +/- 0.6 micro mol.kg(-1).min(-1), respectively; P = 0.001). After a 20-h fast, lipolysis increased to 8.9 +/- 1.5 mmol.kg(-1).min(-1) in NW women (23%), whereas it did not change significantly in obese women (-2%). Fasting decreased insulin concentrations by approximately 30% in both groups, but it did not induce significant changes in leptin concentrations. Mean cortisol concentrations and urinary catecholamine excretion were comparable in both groups. However, mean plasma growth hormone concentrations were higher in NW women than in obese women (1.81 +/- 0.98 compared with 0.74 +/- 0.52 mU/L; P = 0.046). The relative change in lipolysis tended to correlate with mean plasma growth hormone concentrations (r = 0.515, P = 0.059).
  
  
  CONCLUSIONS
  Abdominal obesity-associated hyposomatotropism may be involved in the blunted increase in lipolysis during fasting.
authors.affiliation: Department of General Internal Medicine, Leiden University Medical Center, Leiden, Netherlands. m.m.buijs@lumc.nl
authors.forename: Madelon M
authors.initials: MM
authors.lastname: Buijs
authors.forename: Jacobus
authors.initials: J
authors.lastname: Burggraaf
authors.forename: Carla
authors.initials: C
authors.lastname: Wijbrandts
authors.forename: Marieke L
authors.initials: ML
authors.lastname: de Kam
authors.forename: Marijke
authors.initials: M
authors.lastname: Frölich
authors.forename: Adam F
authors.initials: AF
authors.lastname: Cohen
authors.forename: Johannes A
authors.initials: JA
authors.lastname: Romijn
authors.forename: Hans P
authors.initials: HP
authors.lastname: Sauerwein
authors.forename: A Edo
authors.initials: AE
authors.lastname: Meinders
authors.forename: Hanno
authors.initials: H
authors.lastname: Pijl
mesh_terms: D000005:Abdomen / Q000033:anatomy & histology; D000273:Adipose Tissue / Q000378:metabolism*; D001824:Body Constitution / Q000502:physiology; D015992:Body Mass Index; D016022:Case-Control Studies; D002395:Catecholamines / Q000652:urine; D005215:Fasting / Q000378:metabolism*; D005260:Female; D005990:Glycerol / Q000378:metabolism; D019382:Human Growth Hormone / Q000097:blood / Q000378:metabolism; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007018:Hypopituitarism / Q000097:blood / Q000378:metabolism*; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood; D008066:Lipolysis / Q000502:physiology*; D008875:Middle Aged; D009765:Obesity / Q000097:blood / Q000378:metabolism*; D010084:Oxidation-Reduction; D017698:Postmenopause
chemical_list: D002395:Catecholamines; D007328:Insulin; D020738:Leptin; D019382:Human Growth Hormone; D005990:Glycerol; D006854:Hydrocortisone