The Effect of Physiologic Hyperinsulinemia during an Oral Glucose Tolerance Test on the Levels of Dehydroepiandrosterone (DHEA) and Its Sulfate (DHEAS) in Healthy Young Adults Born with Low and with Normal Birth Weight

Background: Beneficial effects of dehydroepiandrosterone (DHEA) pretreatment were reported in ischaemia/reperfusion (I/R)-induced kidney damage. Methods: To investigate the mechanism of DHEA pretreatment during renal I/R injury, the left renal pedicles of DHEA- [G_DHEA; 4.0 mg/kg/day DHEA dissolved in propylene glycol (PG)] and PG-pretreated male Wistar rats (G_PG) were clamped for 55 min followed by 2 (T₂) and 24 h (T₂₄) of reperfusion. Sham-operated, non-clamped animals (T₀) served as controls in both groups. Renal function, kidney morphology and interleukin 1β (IL-1β), interleukin 6 (IL-6) and vascular endothelial growth factor (VEGF) expression were determined in the kidneys of both groups. Results: Renal functional parameters and kidney structure did not differ in G_DHEA versus G_PG at any time point. Renal mRNA expression of IL-1β was lower at T₀, while IL-6 at T₂ was lower in G_DHEA than in G_PG.While renal VEGF mRNA expression remained unchanged, protein levels were increased at T₂ and T₂₄compared to T₀ kidneys in both groups. VEGF protein levels were lower at T₂ and T₂₄in G_DHEA than in G_PG. Conclusion: We found that DHEA pretreatment alters renal IL-1β, IL-6 and VEGF synthesis. Moreover, contrary changes in VEGF mRNA and protein levels suggest that VEGF synthesis – distinct from other organs – might be primarily posttranscriptionally regulated in postischaemic rat kidneys.

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“…Serum DHEA and dehydroepiandrosterone sulphate (DHEA-S) levels were determined by direct radio-immunoassay as described previously [28] .…”

Section: Serum Biochemistrymentioning

confidence: 99%

Dehydroepiandrosterone Pretreatment Alters the Ischaemia/Reperfusion-Induced VEGF, IL-1 and IL-6 Gene Expression in Acute Renal Failure

Vannay

Fekete²,

Langer³

et al. 2009

Kidney Blood Press Res

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“…We have also shown an increased prevalence of glucose intolerance in women with idiopathic hirsutism, who actually have normal serum androgen levels (12). From another point of view it has been shown that hyperinsulinemia during OGTT might activate the androgen pathway of the adrenal cortex (18). In the present study, we have also investigated the prevalence of glucose intolerance and the presence or absence of insulin resistance in patients with IHA.…”

Section: Discussionmentioning

confidence: 57%

Investigation of adrenal functions in patients with idiopathic hyperandrogenemia

et al. 2006

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Objective: Some patients with hyperandrogenemia had no identifiable cause, which was named as idiopathic hyperandrogenemia (IHA). The role of the adrenal glands in these patients was investigated. Design: Clinical study in patients with IHA at the Endocrinology Department of a University Hospital. Patient(s): In this study, 26 pre-menopausal women with IHA and 20 healthy women were included. Basal hormonal investigations, ACTH test and a 75 g oral glucose tolerance test (OGTT) were performed. Basal levels of total testosterone, free testosterone, androstenedione (A 4 ), sex hormone-binding globulin, DHEA sulfate (DHEAS), cortisol, 17-hydroxyprogesterone (17-OHP), 11-deoxycortisol (11-S) and ACTH-stimulated levels of cortisol, A 4 , DHEAS, 17-OHP, and 11-S were measured. Additionally, glucose and insulin responses to OGTT were obtained. Results: The patients and the control subjects had similar age and body mass index. Peak and area under the curve (AUC) responses of 11-S (P!0.05), DHEAS (P!0.005), and A 4 (peak, P!0.005; AUC, P!0.001) to ACTH test were significantly higher in the patients with IHA than in the control subjects. There was a significant correlation between the basal DHEAS levels, peak 11-S, and AUC 11-S , in response to ACTH-stimulation test in patients with IHA (P!0.005, r, 0.6). Four (16.6%) patients with IHA had glucose intolerance. Conclusion: Our data suggest that adrenal androgen excess may play an important role in patients with IHA and these patients exhibit increased prevalence of glucose intolerance.European Journal of Endocrinology 155 307-311

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“…Recent human studies on the effect of hyperinsulinemia on AA production and metabolism have demonstrated divergent results (33)(34)(35)(36). These results may be due to the variability of the populations studied.…”

Section: Discussionmentioning

confidence: 99%

Effect of sex steroids and insulin on dehydroepiandrosterone sulfate production by hepatoma G2 cells

Pall

Nguyen

Magoffin

et al. 2009

Fertility and Sterility

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OBJECTIVE-To test the hypothesis that DHEAS production from DHEA occurs in hepatic cells, and that this production is augmented by the presence of sex steroids or insulin (INS). DESIGN-In-vitro prospective experimentSETTING-Academic medical center. RESULTS-DHEAS was first detected in the HepG2 cell culture media at 12h incubation. The cumulative production rate of DHEAS increased linearly until 72h incubation. When compared to the effect of treatment with DHEA only, treatment with DHEA plus T, DHT, or E2 delayed the cumulative DHEAS production; alternatively, the addition of INS did not alter DHEAS production. INTERVENTIONS-HepatomaCONCLUSION-These data suggest that while hepatic cells have the ability of converting DHEA to DHEAS, neither sex steroids nor INS result in the increased hepatic production of DHEAS.

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The Effect of Physiologic Hyperinsulinemia during an Oral Glucose Tolerance Test on the Levels of Dehydroepiandrosterone (DHEA) and Its Sulfate (DHEAS) in Healthy Young Adults Born with Low and with Normal Birth Weight

Cited by 8 publications

References 27 publications

Dehydroepiandrosterone Pretreatment Alters the Ischaemia/Reperfusion-Induced VEGF, IL-1 and IL-6 Gene Expression in Acute Renal Failure

Dehydroepiandrosterone Pretreatment Alters the Ischaemia/Reperfusion-Induced VEGF, IL-1 and IL-6 Gene Expression in Acute Renal Failure

Investigation of adrenal functions in patients with idiopathic hyperandrogenemia

Effect of sex steroids and insulin on dehydroepiandrosterone sulfate production by hepatoma G2 cells

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