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Fecal Glucocorticoid Analysis: Non-invasive Adrenal Monitoring in Equids

Fecal Glucocorticoid Analysis: Non-invasive Adrenal Monitoring in Equids

Published on: April 25, 2016

Longitudinal changes in glucocorticoid metabolism are associated with later development of adverse metabolic

Rachel K Crowley¹, Beverly Hughes¹, Joanna Gray¹

¹School of Clinical and Experimental MedicineInstitute of Biomedical Research, Centre for Endocrinology, Diabetes and Metabolism, Queen Elizabeth Hospital, University of Birmingham, Birmingham B15 2TT, UKNIHR/Wellcome Trust Clinical Research FacilityQueen Elizabeth Hospital, Birmingham, UK.

European Journal of Endocrinology

|July 3, 2014

Abstract

Objective:

Dysregulation of enzymes that control local tissue steroid metabolism has been implicated in the pathogenesis of obesity and insulin resistance; however, longitudinal changes in glucocorticoid metabolism have not been investigated. This study was performed to evaluate the role of glucocorticoid metabolism in the development of insulin resistance and obesity and to identify biomarkers for future development of metabolic disease.

Design:

This was a prospective longitudinal observation study conducted over 5 years.

Methods:

A 24-h collection was used to serially analyze urinary glucocorticoid and mineralocorticoid metabolites in 57 obese and overweight patients with no prior diagnosis of diabetes mellitus, recruited from the community.

Results:

Baseline higher 5α-reductase (5αR) activity, but not 11β-hydroxysteroid dehydrogenase type 1 activity, was predictive of increased fasting insulin at final visit (11.4 compared with 7.4 mU/l in subjects with lower 5αR activity, P<0.05), area under the curve insulin response to oral glucose tolerance test (176.7 compared with 89.1 mU/l.h, P<0.01), and homeostasis model assessment (HOMA2-IR; 1.3 compared with 0.8, P<0.01). Higher total glucocorticoid production was associated with abnormal glucose tolerance and increased BMI. During this study, systolic blood pressure increased (equivalent to ∼1 mmHg/year), as did plasma sodium levels; this evidence of increased mineralocorticoid activity was associated with increased aldosterone metabolites and decreased 11β-hydroxysteroid dehydrogenase type 2 activity.

Conclusions:

Increased 5αR activity and glucocorticoid secretion rate over time are linked with the development of metabolic disease, and may represent targets for therapeutic intervention, which merits further study.

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