Literature DB >> 16505229

Effect of nutrient ingestion on total-body and splanchnic cortisol production in humans.

Rita Basu1, Ravinder Singh, Ananda Basu, C M Johnson, Robert A Rizza.   

Abstract

The splanchnic bed produces cortisol at rates approximating extraadrenal tissues by converting cortisone to cortisol via the 11beta-hydroxysteroid dehydrogenase (11beta-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 11beta-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 11beta-HSD type 1 pathway.

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Year:  2006        PMID: 16505229     DOI: 10.2337/diabetes.55.03.06.db05-1335

Source DB:  PubMed          Journal:  Diabetes        ISSN: 0012-1797            Impact factor:   9.461


  11 in total

1.  Determination of cortisol production rates with contemporary liquid chromatography-mass spectrometry to measure cortisol-d(3) dilution after infusion of deuterated tracer.

Authors:  Bethany J Klopfenstein; Jonathan Q Purnell; David D Brandon; Lorne M Isabelle; Andrea E DeBarber
Journal:  Clin Biochem       Date:  2010-12-23       Impact factor: 3.281

2.  Modeling nonsteady-state metabolism from arteriovenous data.

Authors:  Erica Manesso; Gianna M Toffolo; Rita Basu; Robert A Rizza; Claudio Cobelli
Journal:  IEEE Trans Biomed Eng       Date:  2010-12-03       Impact factor: 4.538

3.  Hepatic 11β-hydroxysteroid dehydrogenase type 1 activity in obesity and type 2 diabetes using a novel triple tracer cortisol technique.

Authors:  Simmi Dube; Barbara Norby; Vishwanath Pattan; Ravi K Lingineni; Ravinder J Singh; Rickey E Carter; Ananda Basu; Rita Basu
Journal:  Diabetologia       Date:  2014-04-26       Impact factor: 10.122

4.  Enhanced cortisol production rates, free cortisol, and 11beta-HSD-1 expression correlate with visceral fat and insulin resistance in men: effect of weight loss.

Authors:  Jonathan Q Purnell; Steven E Kahn; Mary H Samuels; David Brandon; D Lynn Loriaux; John D Brunzell
Journal:  Am J Physiol Endocrinol Metab       Date:  2008-12-02       Impact factor: 4.310

Review 5.  Deconstructing the roles of glucocorticoids in adipose tissue biology and the development of central obesity.

Authors:  Mi-Jeong Lee; Pornpoj Pramyothin; Kalypso Karastergiou; Susan K Fried
Journal:  Biochim Biophys Acta       Date:  2013-06-02

Review 6.  11β-hydroxysteroid dehydrogenases: intracellular gate-keepers of tissue glucocorticoid action.

Authors:  Karen Chapman; Megan Holmes; Jonathan Seckl
Journal:  Physiol Rev       Date:  2013-07       Impact factor: 37.312

7.  Increased whole-body and sustained liver cortisol regeneration by 11beta-hydroxysteroid dehydrogenase type 1 in obese men with type 2 diabetes provides a target for enzyme inhibition.

Authors:  Roland H Stimson; Ruth Andrew; Norma C McAvoy; Dhiraj Tripathi; Peter C Hayes; Brian R Walker
Journal:  Diabetes       Date:  2011-01-24       Impact factor: 9.461

8.  Characterization of Cortisol Secretion Rate in Secondary Adrenal Insufficiency.

Authors:  Richard I Dorin; Zhi George Qiao; Matthew Bouchonville; Clifford R Qualls; Ronald M Schrader; Frank K Urban
Journal:  J Endocr Soc       Date:  2017-06-01

9.  The postprandial rise in plasma cortisol in men is mediated by macronutrient-specific stimulation of adrenal and extra-adrenal cortisol production.

Authors:  Roland H Stimson; Nor A Mohd-Shukri; Jennifer L Bolton; Ruth Andrew; Rebecca M Reynolds; Brian R Walker
Journal:  J Clin Endocrinol Metab       Date:  2013-12-20       Impact factor: 5.958

10.  Peripheral and central nervous system inhibition of 11β-hydroxysteroid dehydrogenase type 1 in man by the novel inhibitor ABT-384.

Authors:  D A Katz; W Liu; C Locke; P Jacobson; D M Barnes; R Basu; G An; M J Rieser; D Daszkowski; F Groves; G Heneghan; A Shah; H Gevorkyan; S S Jhee; L Ereshefsky; G J Marek
Journal:  Transl Psychiatry       Date:  2013-08-27       Impact factor: 6.222

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