title: Decreased cortisol production in male type 1 diabetic patients.
abstract: BACKGROUND
  It is unclear whether cortisol production and the 11betaHSD-mediated cortisol to cortisone interconversion are different between type 1 diabetic patients and healthy subjects.
  
  
  METHODS
  Fourteen male, nonobese, normotensive type 1 diabetic patients without severe complications (HbA1c < 8.5%) were studied twice during a daily sodium intake of 50 and 200 mmol, and were then compared with 14 individually matched healthy subjects. Cortisol production was assessed by the sum of urinary cortisol metabolite excretion. Urinary ratios of (tetrahydrocortisol + allo-tetrahydrocortisol)/tetrahydro-cortisone [(THF + allo-THF)/THE] and of free cortisol/free cortisone [UFF/UFE] were determined as parameters of 11betaHSD activity.
  
  
  RESULTS
  Sum of urinary cortisol metabolite excretion during low- and high-salt diet was 7.4 +/- 2.5 vs. 7.7 +/- 2.3 nmol min-1 m-2 (NS) in diabetic patients and 9.7 +/- 2.1 vs. 11.2 +/- 4.1 nmol min-1 m-2 (NS) in healthy subjects, respectively (P < 0.05 vs. healthy subjects at both diets). The allo-THF excretion and allo-THF/THF ratios were lower in the diabetic than in the healthy males during both diets (P < 0.05). Urinary (THF + alloTHF)/THE and UFF/UFE were similar in both groups and remained unchanged after salt loading.
  
  
  CONCLUSIONS
  The sum of urinary cortisol metabolite excretion as a measure of cortisol production is lower in nonobese, normotensive type 1 diabetic males with adequate glycaemic control and without severe complications, irrespective of sodium intake. We suggest that this is at least in part as result of diminished 5alpha reductase activity, resulting in a decreased cortisol metabolic clearance. In type 1 diabetic and in healthy males, the 11betaHSD setpoint is not affected by physiological variations in sodium intake.
authors.affiliation: Department of Endocrinology, University Hospital Groningen, PO Box 30.001, 9700 RB Groningen, the Netherlands. m.n.kerstens@int.azg.nl
authors.forename: M N
authors.initials: MN
authors.lastname: Kerstens
authors.forename: P T
authors.initials: PT
authors.lastname: Luik
authors.forename: F G H
authors.initials: FG
authors.lastname: van der Kleij
authors.forename: A H
authors.initials: AH
authors.lastname: Boonstra
authors.forename: H
authors.initials: H
authors.lastname: Breukelman
authors.forename: W J
authors.initials: WJ
authors.lastname: Sluiter
authors.forename: G J
authors.initials: GJ
authors.lastname: Navis
authors.forename: R P F
authors.initials: RP
authors.lastname: Dullaart
mesh_terms: D042842:11-beta-Hydroxysteroid Dehydrogenases; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D015992:Body Mass Index; D003922:Diabetes Mellitus, Type 1 / Q000378:metabolism* / Q000652:urine; D004305:Dose-Response Relationship, Drug; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism* / Q000652:urine; D006913:Hydroxysteroid Dehydrogenases / Q000378:metabolism* / Q000652:urine; D008297:Male; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage
chemical_list: D001786:Blood Glucose; D017673:Sodium Chloride, Dietary; D006913:Hydroxysteroid Dehydrogenases; D042842:11-beta-Hydroxysteroid Dehydrogenases; D006854:Hydrocortisone