scholarly journals Gender difference in adrenal sensitivity to ACTH is abolished in type 2 diabetes

2015 ◽  
Vol 4 (2) ◽  
pp. 92-99 ◽  
Author(s):  
Lisa Arnetz ◽  
Neda Rajamand Ekberg ◽  
Kerstin Brismar ◽  
Michael Alvarsson

ObjectiveDysfunction of the hypothalamus–pituitary–adrenal (HPA) axis has been implicated in type 2 diabetes (T2D). The aim of this study was to investigate the impact of T2D and gender on the HPA axis.MethodsSynthetic ACTH (1 μg) was administered to 21 subjects with T2D (age 62 (54–70) years, 11 men/ten women, HbA1c 49±2 mmol/mol, treated with diet or oral antidiabetic drugs) and 38 controls (age 58 (41–67) years, 20 men/18 women). Fasting basal B-glucose, serum cortisol, insulin, IGF1 and IGFBP1 concentrations were measured, and sampling for all but IGF1 was repeated 30, 60, and 90 min after ACTH injection. Patients took 0.25 mg dexamethasone at 2200–2300 h and returned the next morning for the measurement of serum cortisol concentration.DesignCross-sectional study.ResultsPatients with T2D had similar fasting serum cortisol, IGF1 and IGFBP1 concentrations; however, serum cortisol concentration after administration of dexamethasone did not differ between the groups. Healthy women exhibited higher peak cortisol levels compared with healthy men (675±26 vs 582±21 nmol/l, P=0.014), while the peak levels were equally high in men and women with T2D, resulting in a higher peak level in men with T2D compared with healthy men (691±42 vs 582±21 nmol/l, P=0.024). Serum cortisol concentration after administration of dexamethasone did not differ between the groups, nor did IGF1 and IGFBP1.Novelty of the findingsSome studies have previously indicated disturbed regulation of the hypothalamus–pituitary–adrenal (HPA) axis in subjects with type 2 diabetes (T2D); however, much remains unknown in this area. To the best of our knowledge, this is the first study to show that the gender difference in the adrenal response to ACTH (with greater reactivity in women) is abolished in T2D. While the clinical implications cannot be determined by this paper, it is known that gender differences exist in the pathogenesis and complications of T2D. Thus, our findings suggest that further research into gender differences in the HPA axis is warranted.ConclusionsGender differences in adrenal response to ACTH were abolished in T2D. Men with T2D had a higher peak cortisol compared with controls. Further studies are needed to elucidate the clinical implications.

1993 ◽  
Vol 136 (1) ◽  
pp. 167-172 ◽  
Author(s):  
S. Crowley ◽  
P. C. Hindmarsh ◽  
J. W. Honour ◽  
C. G. D. Brook

ABSTRACT We compared the reproducibility and repeatability of the acute adrenal response to low doses (90 and 500 ng/1·73 m2) of Synacthen (ACTH(1–24)) with that of the standard dose (250 μg/1·73 m2). We also examined the effect of basal cortisol levels on peak values achieved after stimulation with a low dose. ACTH(1–24) was given to six male volunteers: 90 ng/1·73 m2 twice at 90-min intervals on day 1, and 90 and 500 ng/1·73 m2 once on day 2 and 250 μg/1·73 m2 once on day 3. The rise in serum cortisol concentration with repeated low doses of ACTH was not attenuated (161 ± 49 (s.d.) nmol/l on initial vs 150 ± 41 nmol/l on repeat stimulation; P = 0·5) and this was reproducible (161 ± 49 nmol/l on day 1 vs 148 ± 15 nmol/l on day 2; P = 0·6). A dose of 500 ng ACTH(1–24)/1·73 m2 produced a maximal adrenal response in that the rise in serum cortisol concentration at 20 min was identical with that produced at the same time by the standard dose of 250 μg/1·73 m2. There was a strong positive correlation between the basal cortisol level and peak cortisol concentration after low-dose ACTH stimulation (r = 0·93, P < 0·001) but not between the basal cortisol level and the incremental rise (r= −0·1, P = 0·69). These results suggest that the cortisol response to low-dose ACTH stimulation is reproducible and not attenuated by repeat stimulation at 90-min intervals. The incremental rise in serum cortisol concentration after ACTH stimulation appears constant in these situations and is not influenced by the basal cortisol level. When there is concern that the standard dose may be excessive and mask subtle but important changes in adrenal function, the low dose (500 ng) of ACTH should be used. Journal of Endocrinology (1993) 136, 167–172


2021 ◽  
Vol 23 (08) ◽  
pp. 738-742
Author(s):  
Dr . Dina Ayed Mohammed ◽  

Subject :Diabetes Mellitus (DM) is most common disease characterized by elevation of serum glucose level due to impair insulin production called type 1 DM or impair cell response to insulin called type 2 DM .Cortisol is the steroid hormone that secretion by adrenal gland and it’s consider as stress hormone , act many important role in humane body such as regulation of immune system and metabolic process . Objective of the Study: Role of cortisol in development of DM type 2 disease. Materials and Methods: This study was done on 30 patients with un-control DM type2 patients and 30 control DM type 2 patients , the all subjects age within this study were more than 50 years of both genders .After obtained serum , immediately used quantity method for measured level of serum cortisol concentration . Results: This study shows elevation of serum cortisol concentration level in uncontrol DM type 2 group compare with control DM type 2 group. Conclusion: This study confirms that serum cortisol concentration level can act as support DM type 2 disease .


2018 ◽  
Vol 89 (5) ◽  
pp. 311-319
Author(s):  
Joseph A. Majzoub ◽  
Lisa Swartz Topor

We propose that the normal adrenarche-related rise in dehydroepiandrosterone (DHEA) secretion is ultimately caused by the rise in cortisol production occurring during childhood and adolescent growth, by the following mechanisms. (1) The onset of childhood growth leads to a slight fall in serum cortisol concentration due to growth-induced dilution and a decrease in the negative feedback of cortisol upon ACTH secretion. (2) In response, ACTH rises and stimulates increased cortisol synthesis and secretion in the growing body to restore the serum cortisol concentration to normal. (3) The cortisol concentration produced within and taken up by adrenocortical steroidogenic cells may rise during this time. (4) Cortisol competitively inhibits 3β-hydroxysteroid dehydrogenase type 2 (3βHSD2)-mediated conversion of 17αOH-pregnenolone to cortisol, causing a further fall in serum cortisol, a further decrease in the negative feedback of cortisol upon ACTH, a further rise in ACTH, and further stimulation of adrenal steroidogenesis. (5) The cortisol-mediated inhibition of 3βHSD2 also blocks the conversion of DHEA to androstenedione, causing a rise in adrenal DHEA and DHEA sulfate relative to androstenedione secretion. Thus, the combination of normal body growth plus inhibition of 3βHSD2 by intra-adrenal cortisol may cause normal adrenarche. Childhood obesity may hasten this process by causing a pathologic increase in body size that triggers these same processes at an earlier age, resulting in the premature onset of adrenarche.


1985 ◽  
Vol 54 (04) ◽  
pp. 849-852 ◽  
Author(s):  
O Naesh ◽  
J T Friis ◽  
I Hindberg ◽  
K Winther

SummaryTen patients for elective cholecystectomy were studied pre-, per- and postoperatively. All had neurolept anesthesia. Plasma concentrations of β-TG, TXB2 and 5-HT and intraplatelet 5-HT were measured. Aggregation to ADP was recorded.Serum cortisol concentration was used as index of the stress response, showing peroperative increase and postoperative decrease. Closely related to this we observed a significant increase in P-β-TG and P-TXB2 with postoperative normalization in 6 patients without complications. P-5-HT had a peak peropera-tively and remained elevated postoperatively. A negative correlation between P--5-HT and decreasing intraplatelet 5-HT postoperatively was observed.High postoperative levels of P--5-HT seem to be related to low arterial Po2 and pulmonary dysfunction. In 3 patients with complications a second increase in P-β-TG, P-TXB2 and partly in P--5-HT was found. Platelets were temporarily refractory to ADP immediately following surgery and showed increased aggregabil-ity postoperatively. We conclude that platelets are activated in surgical stress.


2018 ◽  
Author(s):  
Rio-Moreno Mercedes del ◽  
Emilia Alors-Perez ◽  
Antonio Camargo ◽  
Javier Delgado-Lista ◽  
Juan L. Lopez-Canovas ◽  
...  

2009 ◽  
Vol 61 (4) ◽  
pp. 604-611 ◽  
Author(s):  
Jadwiga Piwowarska ◽  
Małgorzata Wrzosek ◽  
Maria Radziwoń-Zaleska ◽  
Beata Ryszewska-Pokraśniewicz ◽  
Michał Skalski ◽  
...  

2018 ◽  
Vol 18 (1) ◽  
Author(s):  
Steven H. Hendriks ◽  
Marco H. Blanker ◽  
Yvonne Roelofsen ◽  
Kornelis J. J. van Hateren ◽  
Klaas H. Groenier ◽  
...  

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