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. 2011 Feb 21;60(3):720–725. doi: 10.2337/db10-0726

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© 2011 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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FIG. 1. — Plasma measurements during deuterated cortisol infusion. Data are means ± SEM for lean control subjects (triangles, n = 7) and obese men with type 2 diabetes (circles, n = 10 for arterial, n = 9 for hepatic vein) with plasma measurements in arterialized (open symbols) and hepatic vein (filled symbols) samples. Cortisol (A), enrichment of cortisol with d4-cortisol (B), and d4-cortisol–to–d3-Cortisol ratios (C). Samples obtained between t = +180 and t = +210 min were used to determine steady-state kinetics. Cortisone (5 mg) was administered orally after 210 min of the deuterated cortisol infusion, and conversion to cortisol was measured over the following 120 min, with the change in d4-cortisol enrichment in the hepatic vein used to measure 11β-HSD1 activity in the liver. By two-way, repeated-measures ANOVA from t = +210 min onwards with time and the two groups as potential factors, the change in d4-cortisol enrichment with time in the hepatic vein was significant in both groups from 10 min after cortisone administration (P < 0.001); there was no significant interaction between subject groups (control vs. obese type 2 diabetic subjects) and time by ANOVA; therefore, post hoc testing was not performed. The d4-cortisol–to–d3-cortisol ratio and total cortisol also increased significantly in the hepatic vein in both groups after oral cortisone (P < 0.01 by ANOVA), again with no difference between groups. Similar changes were observed in arterial samples, again with no difference between groups.