Literature DB >> 34496367

The Association of Cortisol Excretion with Weight and Metabolic Parameters in Nondiabetic Patients with Morbid Obesity.

Johanna Maria Brix1,2, Andrea Tura3, Carsten Thilo Herz4, Astrid Feder1,2, Eva-Christina Krzizek1,2, Verena Parzer1, Giovanni Pacini3, Bernhard Ludvik1,2.   

Abstract

INTRODUCTION: Cortisol is involved in the regulation of gluconeogenesis and glucose utilization. In morbid obesity (MO), the association of cortisol excretion with metabolic parameters is not well-characterized. In our study, we evaluated cortisol excretion in nondiabetic subjects with MO and its effect on glucose metabolism.
METHODS: We included 1,249 nondiabetic patients with MO (79.8% females, mean BMI 44.9 ± 6.5 kg/m2, mean age 38 ± 11 years). Anthropometric data and cardiovascular risk factors were assessed, and an oral glucose tolerance test for calculation of insulin resistance was performed. Cortisol excretion was assessed on 2 consecutive days (24 h urine specimens).
RESULTS: Regarding cortisol excretion, patients were divided into 3 tertiles (urinary cortisol ≤51.6, >51.6 and <117.6, and ≥117.6 μg/24 h, respectively). Patients in the highest tertile were younger (p = 0.003), more obese (BMI: p = 0.040), had lower diastolic blood pressure ([DBP]; p = 0.012), lower total (p = 0.032) and LDL cholesterol (p = 0.021), fasting (p = 0.049) and 2-h glycemia (p = 0.028), 2-h insulinemia (p = 0.020), and HbA1c (p < 0.001), and a higher estimated glomerular filtration rate (eGFR) (p < 0.001). The glucose (p < 0.001) and insulin (p = 0.011) area under the curve (AUC) were also lower. Urinary cortisol excretion adjusted for age, sex, and eGFR was positively correlated with body weight (BW, beta = 0.076, p = 0.004) and overall glucose tolerance (oral disposition index, beta = 0.090, p = 0.011), and negatively with HbA1c (beta = -0.179, p < 0.001), 2-h glycemia (beta = -0.075, p = 0.032), AUC glucose (beta = -0.103, p = 0.002), and DBP (beta = -0.139, p < 0.001). HbA1c, BW, and DBP remained significant after multivariable analysis. DISCUSSION/
CONCLUSION: Despite being more obese, patients with higher cortisol excretion have a more favorable metabolic profile. These results deserve further attention regarding the respective mechanisms.
© 2021 The Author(s). Published by S. Karger AG, Basel.

Entities:  

Keywords:  Bariatric surgery; Cortisol excretion; Morbid obesity

Mesh:

Substances:

Year:  2021        PMID: 34496367      PMCID: PMC8546449          DOI: 10.1159/000517766

Source DB:  PubMed          Journal:  Obes Facts        ISSN: 1662-4025            Impact factor:   3.942


  47 in total

1.  Expression of 11beta-hydroxysteroid dehydrogenase type 1 in adipose tissue is not increased in human obesity.

Authors:  J W Tomlinson; B Sinha; I Bujalska; M Hewison; P M Stewart
Journal:  J Clin Endocrinol Metab       Date:  2002-12       Impact factor: 5.958

Review 2.  Brief review: glucocorticoid excretion in obesity.

Authors:  Karsten Müssig; Thomas Remer; Christiane Maser-Gluth
Journal:  J Steroid Biochem Mol Biol       Date:  2010-01-28       Impact factor: 4.292

3.  Dexamethasone inhibits insulin-stimulated recruitment of GLUT4 to the cell surface in rat skeletal muscle.

Authors:  S P Weinstein; C M Wilson; A Pritsker; S W Cushman
Journal:  Metabolism       Date:  1998-01       Impact factor: 8.694

4.  Insulin sensitivity indices obtained from oral glucose tolerance testing: comparison with the euglycemic insulin clamp.

Authors:  M Matsuda; R A DeFronzo
Journal:  Diabetes Care       Date:  1999-09       Impact factor: 19.112

5.  Tissue-specific changes in peripheral cortisol metabolism in obese women: increased adipose 11beta-hydroxysteroid dehydrogenase type 1 activity.

Authors:  Eva Rask; Brian R Walker; Stefan Söderberg; Dawn E W Livingstone; Mats Eliasson; Owe Johnson; Ruth Andrew; Tommy Olsson
Journal:  J Clin Endocrinol Metab       Date:  2002-07       Impact factor: 5.958

Review 6.  11beta-hydroxysteroid dehydrogenase type 1: a tissue-specific regulator of glucocorticoid response.

Authors:  Jeremy W Tomlinson; Elizabeth A Walker; Iwona J Bujalska; Nicole Draper; Gareth G Lavery; Mark S Cooper; Martin Hewison; Paul M Stewart
Journal:  Endocr Rev       Date:  2004-10       Impact factor: 19.871

7.  Association of 24-hour cortisol production rates, cortisol-binding globulin, and plasma-free cortisol levels with body composition, leptin levels, and aging in adult men and women.

Authors:  Jonathan Q Purnell; David D Brandon; Lorne M Isabelle; D Lynn Loriaux; Mary H Samuels
Journal:  J Clin Endocrinol Metab       Date:  2004-01       Impact factor: 5.958

Review 8.  Regulation of Glucose Homeostasis by Glucocorticoids.

Authors:  Taiyi Kuo; Allison McQueen; Tzu-Chieh Chen; Jen-Chywan Wang
Journal:  Adv Exp Med Biol       Date:  2015       Impact factor: 2.622

Review 9.  Clinical review: The pathogenetic role of cortisol in the metabolic syndrome: a hypothesis.

Authors:  Panagiotis Anagnostis; Vasilios G Athyros; Konstantinos Tziomalos; Asterios Karagiannis; Dimitri P Mikhailidis
Journal:  J Clin Endocrinol Metab       Date:  2009-05-26       Impact factor: 5.958

10.  Glucocorticoids Reprogram β-Cell Signaling to Preserve Insulin Secretion.

Authors:  Nicholas H F Fine; Craig L Doig; Yasir S Elhassan; Nicholas C Vierra; Piero Marchetti; Marco Bugliani; Rita Nano; Lorenzo Piemonti; Guy A Rutter; David A Jacobson; Gareth G Lavery; David J Hodson
Journal:  Diabetes       Date:  2017-12-04       Impact factor: 9.461

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