Faculty Opinions recommendation of 11beta-Hydroxysteroid Dehydrogenase Type 1 Regulation by Intracellular Glucose 6-Phosphate Provides Evidence for a Novel Link between Glucose Metabolism and Hypothalamo-Pituitary-Adrenal Axis Function.

To evaluate the effects of altered corticosteroid metabolism on the hypothalamic-pituitary-adrenal axis, we examined rats treated with glycyrrhizic acid (G rats) or rifampicin (R rats) for 7 days. The half-life of exogenously administered hydrocortisone as a substitute for corticosterone was longer in G rats and shorter in R rats, with no differences in basal plasma levels of ACTH or corticosterone. The ACTH responses to human corticotropin-releasing factor (CRF) or insulin-induced hypoglycemia were greater in G rats and tended to be smaller in R rats compared with those in the control rats, whereas the corticosterone response was similar. No difference was observed in the content and mRNA level of hypothalamic CRF among the groups. The number and mRNA level of CRF receptor and type 1 11β-hydroxysteroid dehydrogenase (11-HSD1) mRNA level in the pituitary were increased in G rats but not changed in R rats, suggesting that chronically increased intrapituitary corticosterone upregulates pituitary CRF receptor expression. In contrast, CRF mRNA levels in the pituitary were increased in R rats. Our data indicate novel mechanisms of corticosteroid metabolic modulation and the involvement of pituitary 11-HSD1 and CRF in glucocorticoid feedback physiology.

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The hypothalamus–pituitary–adrenal axis in patients with CRPS type 1: molar cortisol to DHEA ratio increases with disease duration

European Journal of Psychotraumatology ◽

10.3402/ejpt.v3i0.19395 ◽

2012 ◽

Vol 3 (0) ◽

Author(s):

Jai Y. Park ◽

Ryun S. Ahn

Keyword(s):

Disease Duration ◽

Adrenal Axis ◽

Hypothalamus Pituitary Adrenal Axis ◽

Pituitary Adrenal Axis

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Altered Cortisol Metabolism Increases Nocturnal Cortisol Bioavailability in Prepubertal Children With Type 1 Diabetes Mellitus

Frontiers in Endocrinology ◽

10.3389/fendo.2021.742669 ◽

2021 ◽

Vol 12 ◽

Author(s):

Julie Brossaud ◽

Jean-Benoît Corcuff ◽

Vanessa Vautier ◽

Aude Bergeron ◽

Aurelie Valade ◽

...

Keyword(s):

Diabetes Mellitus ◽

Type 1 Diabetes ◽

Hpa Axis ◽

Trait Anxiety ◽

Hydroxysteroid Dehydrogenase ◽

Prepubertal Children ◽

Cortisol Metabolism ◽

Hypothalamus Pituitary Adrenal Axis ◽

Pituitary Adrenal Axis

ObjectiveDisturbances in the activity of the hypothalamus-pituitary-adrenal axis could lead to functional alterations in the brain of diabetes patients. In a later perspective of investigating the link between the activity of the hypothalamus-pituitary-adrenal axis and the developing brain in children with diabetes, we assessed here nocturnal cortisol metabolism in prepubertal children with type 1 diabetes mellitus (T1DM).MethodsPrepubertal patients (aged 6–12 years) diagnosed with T1DM at least 1 year previously were recruited, along with matched controls. Nocturnal urine samples were collected, with saliva samples taken at awakening and 30 minutes after awakening. All samples were collected at home over 5 consecutive days with no detectable nocturnal hypoglycaemia. The State-Trait Anxiety Inventory (trait scale only) and Child Depression Inventory were also completed. Glucocorticoid metabolites in the urine, salivary cortisol (sF) and cortisone (sE) were measured by liquid chromatography–tandem mass spectrometry. Metabolic data were analysed by logistic regression, adjusting for sex, age, BMI and trait anxiety score.ResultsUrine glucocorticoid metabolites were significantly lower in T1DM patients compared to controls. 11β-hydroxysteroid dehydrogenase type 1 activity was significantly higher, while 11β-hydroxysteroid dehydrogenase type 2, 5(α+β)-reductase and 5α-reductase levels were all lower, in T1DM patients compared to controls. There was a significant group difference in delta sE level but not in delta sF level between the time of awakening and 30 minutes thereafter.ConclusionsOur findings suggest that altered nocturnal cortisol metabolism and morning HPA axis hyperactivity in children with T1DM leads to greater cortisol bioavailability and lower cortisol production as a compensatory effect. This altered nocturnal glucocorticoid metabolism when cortisol production is physiologically reduced and this HPA axis hyperactivity question their impact on brain functioning.

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Lack of Association of the 11β-Hydroxysteroid Dehydrogenase Type 1 Gene 83,557insA and Hexose-6-Phosphate Dehydrogenase Gene R453Q Polymorphisms with Body Composition, Adrenal Androgen Production, Blood Pressure, Glucose Metabolism, and Dementia

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jc.2006-1349 ◽

2007 ◽

Vol 92 (1) ◽

pp. 359-362 ◽

Cited By ~ 22

Author(s):

Pauline Smit ◽

Marieke J. H. J. Dekker ◽

Frank Jan de Jong ◽

Annewieke W. van den Beld ◽

Jan W. Koper ◽

...

Keyword(s):

Blood Pressure ◽

Body Composition ◽

Glucose Metabolism ◽

Hydroxysteroid Dehydrogenase ◽

Adrenal Androgen ◽

Dehydrogenase Gene

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Distinct Effect of Stress on 11β-Hydroxysteroid Dehydrogenase Type 1 and Corticosteroid Receptors in Dorsal and Ventral Hippocampus

Physiological Research ◽

10.33549/physiolres.932588 ◽

2014 ◽

pp. 255-261 ◽

Cited By ~ 1

Author(s):

P. ERGANG ◽

A. KUŽELOVÁ ◽

M. SOTÁK ◽

P. KLUSOŇOVÁ ◽

J. MAKAL ◽

...

Keyword(s):

Feedback Inhibition ◽

Dorsal Hippocampus ◽

Active Form ◽

Hydroxysteroid Dehydrogenase ◽

Ventral Hippocampus ◽

Corticosteroid Receptors ◽

Ca1 Region ◽

Strain Stress ◽

Pituitary Adrenal Axis

Multiple lines of evidence suggest the participation of the hippocampus in the feedback inhibition of the hypothalamus-pituitary-adrenal axis during stress response. This inhibition is mediated by glucocorticoid feedback due to the sensitivity of the hippocampus to these hormones. The sensitivity is determined by the expression of glucocorticoid (GR) and mineralocorticoid (MR) receptors and 11β-hydroxysteroid dehydrogenase type 1 (11HSD1), an enzyme that regulates the conversion of glucocorticoids from inactive to active form. The goal of our study was to assess the effect of stress on the expression of 11HSD1, GR and MR in the ventral and dorsal region of the CA1 hippocampus in three different rat strains with diverse responses to stress: Fisher 344, Lewis and Wistar. Stress stimulated 11HSD1 in the ventral but not dorsal CA1 hippocampus of Fisher 344 but not Lewis or Wistar rats. In contrast, GR expression following stress was decreased in the dorsal but not ventral CA1 hippocampus of all three strains. MR expression was not changed in either the dorsal or ventral CA1 region. These results indicate that (1) depending on the strain, stress stimulates 11HSD1 in the ventral hippocampus, which is known to be involved in stress and emotion reactions whereas (2) independent of strain, stress inhibits GR in the dorsal hippocampus, which is predominantly involved in cognitive functions.

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