Publication:
Cortisol Metabolism in Obese Women with Normal and Impaired Glucose Tolerance

dc.contributor.authorKAĞAN GÜNGÖR
dc.contributor.authornur dokuzeylul gungor
dc.contributor.authorMUSTAFA SAIT GONEN
dc.contributor.institutionİSTANBUL MEDENİYET ÜNİVERSİTESİ
dc.contributor.institutionBAHÇEŞEHİR ÜNİVERSİTESİ
dc.contributor.institutionİSTANBUL ÜNİVERSİTESİ - CERRAHPAŞA
dc.date.accessioned2025-09-20T19:57:26Z
dc.date.issued2021
dc.date.submitted17.05.2022
dc.description.abstractObjectives: Increases in fasting plasma cortisol level in the morning has been associated with glucose intolerance and insulin resistance in patients with metabolic syndrome. This study investigated the relationship between fasting morning cortisol and insulin resistance defined by homeostasis model assessment for insulin resistance (HOMA-IR) in obese women with normal glucose tolerance (NGT) and impaired glucose tolerance (IGT). Methods: The study was carried out in the Obesity outpatient clinic between June and September 2005. Total body fat mass, lean body mass, total body fluid, and basal metabolic rate were calculated via bioelectrical impedance analysis. Body mass index (BMI), fasting plasma glucose, insulin, HOMA-IR, basal cortisol, 24-h urinary free cortisol, overnight dexamethasone suppression test, lipids, oral glucose tolerance test results, and thyroid function tests were obtained from patient files in the obesity clinic. Results: This study included 38 obese women, 21 (55.3%) of which had NGT. There was no significant difference between NGT and IGT cases in terms of age, BMI, waist circumference, insulin, HOMA-IR, basal cortisol, and 24-h urinary free cortisol (p=0.484, p=0.399, p=0.517, p=0.639, p=0.973, p=0.758, p=0.161, respectively). There was no correlation between basal cortisol levels in patients with NGT, however, there was a moderate correlation between basal cortisol and HOMA-IR in patients with IGT (p=0.464, r=0.629 and p=0.007). Conclusion: Although the basal cortisol levels of NGT and IGT patients were similar, a moderate correlation exists between basal cortisol and HOMA-IR in patients with IGT.
dc.identifier.doi10.5505/anatoljfm.2021.46036
dc.identifier.endpage242
dc.identifier.issn2630-5593
dc.identifier.issn2651-3455
dc.identifier.issue3
dc.identifier.startpage238
dc.identifier.urihttps://hdl.handle.net/20.500.14719/4848
dc.identifier.volume4
dc.language.isoen
dc.relation.journalThe anatolian journal of family medicine (Online)
dc.subjectEndokrinoloji ve Metabolizma
dc.subjectGenel ve Dahili Tıp
dc.titleCortisol Metabolism in Obese Women with Normal and Impaired Glucose Tolerance
dc.typeResearch Article
dcterms.references1. Salehi M, Ferenczi A, Zumoff B. Obesity and cortisol status. Horm Metab Res 2005,37(4):193–7.,2. Zumoff B, Fukushima DK, Hellman L. Intercomparison of four methods for measuring cortisol production. J Clin Endocrinol Metab 1974,38(2):169–75.,3. Jessop DS, Dallman MF, Fleming D, Lightman SL. Resistance to glucocorticoid feedback in obesity. J Clin Endocrinol Metab 2001,86(9):4109–14.,4. Rask E, Walker BR, Söderberg S, Livingstone DE, Eliasson M, Johnson O, et al. Tissue-specific changes in peripheral cortisol metabolism in obese women: increased adipose 11beta-hydroxysteroid dehydrogenase type 1 activity. J Clin Endocrinol Metab 2002,87(7):3330–6.,5. Masuzaki H, Paterson J, Shinyama H, Morton NM, Mullins JJ, Seckl JR, et alk. A transgenic model of visceral obesity and the metabolic syndrome. Science 2001,294(5549):2166–70.,6. Ljung T, Andersson B, Bengtsson BA, Björntorp P, Mårin P. Inhibition of cortisol secretion by dexamethasone in relation to body fat distribution: a dose-response study. Obes Res 1996,4:277–82.,7. Scaroni C, Albiger NM, Palmieri S, Iacuaniello D, Graziadio C, Damiani L, et al, Altogether to Beat Cushing’s Syndrome (ABC) study group. Approach to patients with pseudo-Cushing's states. Endocr Connect 2020,9(1):R1–R13.,8. Björntorp P, Rosmond R. The metabolic syndrome--a neuroendocrine disorder? Br J Nutr 2000,83(Suppl 1):S49–57.,9. Dos Santos ML, Aragon FF, Padovani CR, Pimenta WP. Daytime variations in glucose tolerance in people with impaired glucose tolerance. Diabetes Res Clin Pract 2006,74(3):257–62.,10. Tchernof A, Després JP. Pathophysiology of human visceral obesity: an update. Physiol Rev 2013,93(1):359–404.,11. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985,28(7):412–9.,12. Sainaghi PP, Castello L, Bergamasco L, Carnevale Schianca GP, Bartoli E. Metabolic characteristics of glucose intolerance: the critical role of obesity. Exp Clin Endocrinol Diabetes 2008,116(2):86–93.,13. Christiansen JJ, Djurhuus CB, Gravholt CH, Iversen P, Christiansen JS, Schmitz O, et al. Effects of cortisol on carbohydrate, lipid, and protein metabolism: studies of acute cortisol withdrawal in adrenocortical failure. J Clin Endocrinol Metab 2007,92(9):3553–9.,14. Reynolds RM, Walker BR, Syddall HE, Whorwood CB, Wood PJ, Phillips DI. Elevated plasma cortisol in glucose-intolerant men: differences in responses to glucose and habituation to venepuncture. J Clin Endocrinol Metab 2001,86(3):1149–53.,15. Gerards J, Heinrich DA, Adolf C, Meisinger C, Rathmann W, Sturm L, et al. Impaired glucose metabolism in primary aldosteronism is associated with cortisol cosecretion. J Clin Endocrinol Metab 2019,104(8):3192–202.,16. Praveen EP, Sahoo JP, Kulshreshtha B, Khurana ML, Gupta N, Dwivedi SN, et al. Morning cortisol is lower in obese individuals with normal glucose tolerance. Diabetes Metab Syndr Obes 2011,4:347–52.,17. Ward AM, Fall CH, Stein CE, Kumaran K, Veena SR, Wood PJ, et al. Cortisol and the metabolic syndrome in South Asians. Clin Endocrinol (Oxf) 2003,58(4):500–5.,18. Pasquali R, Cantobelli S, Casimirri F, Capelli M, Bortoluzzi L, Flamia R, et al. The hypothalamic-pituitary-adrenal axis in obese women with different patterns of body fat distribution. J Clin Endocrinol Metab 1993,77(2):341–6.,19. Rosmond R, Dallman MF, Björntorp P. Stress-related cortisol secretion in men: relationships with abdominal obesity and endocrine, metabolic and hemodynamic abnormalities. J Clin Endocrinol Metab 1998,83(6):1853–9.,20. Andrew R, Phillips DI, Walker BR. Obesity and gender influence cortisol secretion and metabolism in man. J Clin Endocrinol Metab 1998,83(5):1806–9.,21. Newel-Price JDC, Auchus RJ. The adrenal cortex. In: Melmed S, Auchus RJ, Goldfine A, Koenig R, Rosen C, editors. Williams Textbook of Endocrinology. 14th ed., Philadelphia: Elsevier, 2020. p. 480–541.,22. Sookoian S, Gemma C, Fernández Gianotti T, Burgueño A, Alvarez A, González CD, et al. Effects of rotating shift work on biomarkers of metabolic syndrome and inflammation. J Intern Med 2007,261(3):285–92.,23. Shi SQ, Ansari TS, McGuinness OP, Wasserman DH, Johnson CH. Circadian disruption leads to insulin resistance and obesity. Curr Biol 2013,23(5):372–81.,24. Albrecht U. The circadian clock, metabolism and obesity. Obes Rev 2017,18(Suppl 1):25–33.
dspace.entity.typePublication
local.indexed.atTRDizin

Files