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Effect of Nutrient Ingestion on Total-Body and Splanchnic Cortisol Production in Humans

¹ Division of Endocrinology, Metabolism and Nutrition, Mayo Clinic, Rochester, Minnesota
² Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota
³ Department of Vascular and Interventional Radiology, Mayo Clinic, Rochester, Minnesota

Address correspondence and reprint requests to Robert A. Rizza, MD, Mayo Clinic, 200 1st St. SW, Rm. 5-194 Joseph, Rochester, MN 55905. E-mail: rizza.robert{at}mayo.edu

Abbreviations: 11ß-HSD, 11ß-hydroxysteroid dehydrogenase

The splanchnic bed produces cortisol at rates approximating extraadrenal tissues by converting cortisone to cortisol via the 11ß-hydroxysteroid dehydrogenase (11ß-HSD) type 1 pathway. It is not known whether splanchnic cortisol production is regulated by nutrient ingestion and/or by the accompanying changes in hormone secretion. To address this question, 18 healthy humans were randomized to ingest either a mixed meal or to receive an intravenous saline infusion while total-body, splanchnic, and D₃ cortisol production (an index of 11ß-HSD type 1 activity) were measured using the combined hepatic catheterization and D₄ cortisol infusion methods. Fasting glucose and insulin concentrations did not differ on the meal and saline study days. Glucose and insulin concentrations increased after meal ingestion, peaking at 11.0 ± 1.0 mmol/l and 451 ± 64 pmol/l, respectively, at 45 min, then fell to baseline thereafter. In contrast, glucose and insulin concentrations slowly fell to 5.1 ± 0.1 mmol/l and 27 ± 6 pmol/l during the 6 h of observation on the saline study day. Fasting cortisol concentration did not differ on the meal and saline study days. Cortisol increased (P < 0.05) to a peak of 353 ± 55 nmol/l after meal ingestion but did not change after saline infusion. The increase in cortisol after meal ingestion was associated with an increase in both total body cortisol (from 748 ± 63 to 1,620 ± 235 nmol/min; P < 0.01) and total body D₃ cortisol (from 99 ± 11 to 143 ± 11 nmol/min; P < 0.01) production, whereas there was no change in either on the saline study day. The increase in total-body cortisol and D₃ cortisol production after meal ingestion originated in extrasplanchnic tissues since splanchnic cortisol production (mean 0–360 min: 254 ± 83 vs. 262 ± 36 nmol/min) and splanchnic D₃ cortisol production (mean 0–360 min: 72 ± 22 vs. 77 ± 14 nmol/min) did not differ on the meal and saline study days. We conclude that ingestion of a mixed meal does not alter either splanchnic cortisol production or the conversion of D₄ cortisol to D₃ cortisol or, therefore by implication, flux via the splanchnic 11ß-HSD type 1 pathway.

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