title: Glucose ingestion selectively amplifies ACTH and cortisol secretory-burst mass and enhances their joint synchrony in healthy men.
abstract: BACKGROUND
  Glucose intake is associated with a variable increase in adrenal glucocorticoid secretion.
  
  
  OBJECTIVE
  Glucose ingestion elevates cortisol secretion by 1) augmenting pulsatile ACTH release; and/or 2) enhancing ACTH-cortisol synchrony or dose-responsiveness.
  
  
  METHODS
  Fifty-eight healthy men ages 19-78 yr with computed tomography-estimated abdominal visceral fat participated in the study.
  
  
  METHODS
  The study was conducted at the Clinical Translational-Research Center and Veterans Affairs Medical Center.
  
  
  METHODS
  We conducted frequent sampling of plasma ACTH and cortisol concentrations after glucose vs. water ingestion in the fasting state, as well as deconvolution, approximate entropy, linear-regression, and dose-response analysis.
  
  
  RESULTS
  After water ingestion, age was a negative correlate of the mass of ACTH (P = 0.009; R(2) = 0.119) and of cortisol (P < 0.001; R(2) = 0.269) secreted per burst. Glucose ingestion abolished both relationships but amplified pulsatile ACTH (P = 0.009) and cortisol (P = 0.001) secretion. Glucose exposure selectively augmented the mass of ACTH (P < 0.001) and of cortisol (P = 0.004) secreted per burst without altering burst number or basal secretion. The increment in pulsatile ACTH strongly predicted the increment in pulsatile cortisol (P < 10(-4); R(2) = 0.325) secretion. Abdominal visceral fat positively forecast the glucose-induced increment in cortisol secretory-burst mass (P = 0.019). According to approximate entropy analysis, glucose input also enhanced the joint synchrony of ACTH-cortisol secretory patterns (P ≤ 0.001). Caloric intake did not affect analytical dose-response estimates of ACTH potency and efficacy or adrenal sensitivity.
  
  
  CONCLUSIONS
  Conjoint augmentation of the mass of ACTH and cortisol secreted per burst and enhancement of ACTH-cortisol synchrony underlie glucose-induced glucocorticoid secretion in healthy men. Visceral adiposity is a predictor of the glucose-stimulated increment in burst-like cortisol output, suggesting an additional possible mechanism for increased cardiovascular risk in abdominal obesity.
authors.affiliation: Endocrine Section, Medical Service, Salem Veterans Affairs Medical Center, Salem, Virginia 24153, USA.
authors.forename: Ali
authors.initials: A
authors.lastname: Iranmanesh
authors.forename: Donna
authors.initials: D
authors.lastname: Lawson
authors.forename: Barbara
authors.initials: B
authors.lastname: Dunn
authors.forename: Johannes D
authors.initials: JD
authors.lastname: Veldhuis
mesh_terms: D000284:Administration, Oral; D000324:Adrenocorticotropic Hormone / Q000097:blood / Q000378:metabolism*; D000328:Adult; D000368:Aged; D005947:Glucose / Q000008:administration & dosage*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood / Q000378:metabolism*; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects* / Q000502:physiology; D008297:Male; D008875:Middle Aged; D010913:Pituitary-Adrenal System / Q000187:drug effects* / Q000502:physiology
chemical_list: D000324:Adrenocorticotropic Hormone; D005947:Glucose; D006854:Hydrocortisone