title: Dysregulation of the autonomic nervous system can be a link between visceral adiposity and insulin resistance.
abstract: OBJECTIVE
  To evaluate the interplay among abdominal adipose tissue distribution, the cortisol axis, the autonomic nervous system, and insulin resistance.
  
  
  METHODS
  Two age-, sex-, and BMI-matched groups were studied. Fifteen subjects were first-degree relatives of patients with type 2 diabetes (R), and 15 had no family history of diabetes (controls, C). A hyperinsulinemic euglycemic clamp, cortisol measurements, and analysis of heart rate variability (HRV) were performed. Computed tomography was performed in a subgroup (n = 9 + 9) to determine abdominal adipose tissue distribution.
  
  
  RESULTS
  R tended to be less insulin-sensitive than C (M value 9.2 +/- 1.0 vs 10.3 +/- 0.7 mg/kg per minute, not significant). Stimulation with tetracosactin or corticotropin releasing hormone yielded lower peak serum cortisol levels in R (p = 0.03 and p = 0.06, respectively). The amount of visceral abdominal fat (VAT) tended to be greater in R. In all subjects, VAT was negatively correlated to insulin sensitivity (r = -0.93, p < 0.001). There was a positive association between VAT and resting heart rate (r = 0.70, p = 0.003) and sympathetic/parasympathetic ratio in HRV assessment after tilt (r = 0.53, p = 0.03). Subcutaneous abdominal tissue was not associated with insulin sensitivity or any of the hormonal or HRV assessments.
  
  
  CONCLUSIONS
  Subjects genetically predisposed for type 2 diabetes had a tendency toward a larger amount of VAT and to lower insulin sensitivity compared with control subjects. The amount of visceral fat was strongly associated with insulin resistance and signs of a high ratio of sympathetic vs. parasympathetic reactivity. A large amount of visceral fat may act in concert with sympathetic/parasympathetic imbalance to promote the development of insulin resistance, and this may be partly independent of genetic background.
authors.affiliation: Department of Medicine, Umeå University Hospital, S-901 85 Umeå, Sweden. stina.lindmark@medicin.umu.se
authors.forename: Stina
authors.initials: S
authors.lastname: Lindmark
authors.forename: Lars
authors.initials: L
authors.lastname: Lönn
authors.forename: Urban
authors.initials: U
authors.lastname: Wiklund
authors.forename: Magnus
authors.initials: M
authors.lastname: Tufvesson
authors.forename: Tommy
authors.initials: T
authors.lastname: Olsson
authors.forename: Jan W
authors.initials: JW
authors.lastname: Eriksson
mesh_terms: D000273:Adipose Tissue; D000324:Adrenocorticotropic Hormone; D000328:Adult; D001341:Autonomic Nervous System / Q000503:physiopathology*; D001786:Blood Glucose / Q000032:analysis; D001823:Body Composition; D015992:Body Mass Index; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics / Q000503:physiopathology; D005260:Female; D015309:Glucose Clamp Technique; D005951:Glucose Tolerance Test; D006339:Heart Rate; D006706:Homeostasis; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000235:genetics; D008297:Male; D012044:Regression Analysis; D014781:Viscera
chemical_list: D001786:Blood Glucose; D007328:Insulin; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone