title: Obesity and type 2 diabetes do not alter splanchnic cortisol production in humans.
abstract: BACKGROUND
  Cortisol is a potent regulator of carbohydrate, fat, and protein metabolism.
  
  
  OBJECTIVE
  The objective of the study was to determine whether obesity alone or in combination with type 2 diabetes increases splanchnic and/or leg cortisol production.
  
  
  METHODS
  Splanchnic and leg cortisol production were measured using the hepatic and leg catheterization technique combined with infusion of D4-cortisol.
  
  
  METHODS
  The study was conducted in a General Clinical Research Center.
  
  
  METHODS
  Nine lean nondiabetic, 10 obese nondiabetic, and 11 obese diabetic subjects were studied.
  
  
  METHODS
  Diabetic volunteers were withdrawn from their glucose-lowering medications before study.
  
  
  METHODS
  Rates of total body, splanchnic and leg cortisol, and D3-cortisol production were measured.
  
  
  RESULTS
  Rates of splanchnic cortisol production equaled or exceeded those occurring in extrasplanchnic tissues (e.g. the adrenals) in all three groups. However, because concurrent splanchnic cortisol uptake also occurred, net splanchnic cortisol release was minimal. Splanchnic cortisol production and splanchnic D3-cortisol production (an index of splanchnic 11beta-hydroxysteroid dehydrogenase type 1 activity) did not differ among the three groups. In addition, splanchnic cortisol production did not correlate with either visceral fat or endogenous glucose production. On the other hand, splanchnic cortisol uptake was greater in the obese diabetic than lean nondiabetic subjects (25 +/- 2.9 vs. 15.3 +/- 2.5 microg/min; P < 0.05). Splanchnic, but not leg, D3-cortisol production was correlated with total body D3-cortisol production (r = 0.70; P < 0.001).
  
  
  CONCLUSIONS
  Although large amounts of cortisol are produced within the splanchnic bed, implying high intrahepatic glucocorticoid concentrations, rates do not differ in lean and obese nondiabetic humans and are not influenced by the presence of type 2 diabetes mellitus. On the other hand, obesity but not diabetes increases splanchnic cortisol uptake.
authors.affiliation: Division of Endocrinology, Metabolism, and Nutrition, Mayo Clinic, 200 1st Street SW, Room 5-194 Joseph, Rochester, Minnesota 55905, USA.
authors.forename: Rita
authors.initials: R
authors.lastname: Basu
authors.forename: Ravinder J
authors.initials: RJ
authors.lastname: Singh
authors.forename: Ananda
authors.initials: A
authors.lastname: Basu
authors.forename: Elizabeth G
authors.initials: EG
authors.lastname: Chittilapilly
authors.forename: Michael C
authors.initials: MC
authors.lastname: Johnson
authors.forename: Gianna
authors.initials: G
authors.lastname: Toffolo
authors.forename: Claudio
authors.initials: C
authors.lastname: Cobelli
authors.forename: Robert A
authors.initials: RA
authors.lastname: Rizza
mesh_terms: D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1 / Q000502:physiology; D000328:Adult; D000368:Aged; D003348:Cortisone / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism*; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000096:biosynthesis*; D007866:Leg; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000378:metabolism*; D013152:Splanchnic Circulation / Q000502:physiology*
chemical_list: D005230:Fatty Acids, Nonesterified; D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1; D003348:Cortisone; D006854:Hydrocortisone