Alterations in urinary cortisol metabolism in Japanese patients with type 2 diabetes mellitus

  • Endoh Tatsuji
    Department of Endocrinology, Metabolism and Diabetes, Kinki University School of Medicine
  • Ohno Yasuhiro
    Department of Endocrinology, Metabolism and Diabetes, Kinki University School of Medicine
  • Hoshiro Madoka
    Department of Endocrinology, Metabolism and Diabetes, Kinki University School of Medicine
  • Aoki Norihiko
    Department of Endocrinology, Metabolism and Diabetes, Kinki University School of Medicine

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Objective: Urinary cortisol metabolites were measured in type 2 diabetes patients and control subjects to determine whether type 2 diabetes mellitus and obesity are associated with a derangement in cortisol metabolism. Material and methods: Urine sample from 33 patients with type 2 diabetes and 35 control subjects were studied. Six cortisol metabolites were measured in urine collected over a 24 hour period: cortisol (UFF) 6β-hydroxycortisol (6β-OHF), and cortisone (UFE) were measured by high-performance liquid chromatography (HPLC); tetrahydrocortisol (THF), allo-tetrahydrocortisol (allo-THF) and tetrahydrocortisone (THE) were measured by HPLC mass spectrometry/mass spectrometry (LC-MS/MS) Results: Both urinary 6β-OHF and UFE correlated positively with the body mass index (BMI) among diabetics (p<0.005 and P<0.05, respectively), UFF and UFF/UFE ratio did not. The only metabolite to correlate with BMI in the controls was 6β-OHF, and the correlation was weak (p<0.01). The ratio of urinary THF+allo-THF to THE was significantly lower in the diabetic patients than the control subjects. The ratio of urinary THF+allo-THF to THE was negatively correlated with HbAlc in the diabetic patients (p<0.01). Conclusions: Urinary 6β-OHF had the strongest correlation with body mass index in type 2 diabetes mellitus, followed by urinary free cortisone. No correlation was found between urinary free cortisol and body mass index in normal controls, however, the ratio of urinary THF+allo-THF to THE was negatively correlated with HbAlc, suggesting that down-regulation of the conversion of cortisone to cortisol induced by 11β-hydroxysteroid dehydrogenase type 1 might be enhanced in chronic hyperglycemia. If there is such an enhancement, a compensatory mechanism to reduce the generation of cortisol may be at work in diabetes mellitus.

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