Abnormal Results of Dexamethasone Suppression Tests in Nondepressed Patients With Diabetes Mellitus

Hudson, James I.; Hudson, Margo; Rothschild, Anthony J.; Vignati, Louis; Schatzberg, Alan F.; Melby, James C.

doi:10.1001/archpsyc.1983.01790220076012

Cited by 95 publications

(51 citation statements)

References 19 publications

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“…DM2 patients have elevated basal ACTH levels (Vermes et al 1985, Chiodini et al 2006) and high cortisol levels, both basal and after Dex suppression (Hudson et al 1984, Prpić-Križevac et al 2012. In this regard, the activity of the HPA axis is enhanced in diabetic patients with asymptomatic autonomic imbalance due to prevalent parasympathetic failure.…”

Section: Hpa In Diabetesmentioning

confidence: 99%

Stressing diabetes? The hidden links between insulinotropic peptides and the HPA axis

Diz-Chaves

Gil‐Lozano

Toba

et al. 2016

Journal of Endocrinology

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Diabetes mellitus exerts metabolic stress on cells and it provokes a chronic increase in the long-term activity of the hypothalamus-pituitary-adrenocortical (HPA) axis, perhaps thereby contributing to insulin resistance. GLP-1 receptor (GLP-1R) agonists are pleiotropic hormones that not only affect glycaemic and metabolic control, but they also produce many other effects including activation of the HPA axis. In fact, several of the most relevant effects of GLP-1 might involve, at least in part, the modulation of the HPA axis. Thus, the anorectic activity of GLP-1 could be mediated by increasing CRF at the hypothalamic level, while its lipolytic effects could imply a local increase in glucocorticoids and glucocorticoid receptor (GC-R) expression in adipose tissue. Indeed, the potent activation of the HPA axis by GLP-1R agonists occurs within the range of therapeutic doses and with a short latency. Interestingly, the interactions of GLP-1 with the HPA axis may underlie most of the effects of GLP-1 on food intake control, glycaemic metabolism, adipose tissue biology and the responses to stress. Moreover, such activity has been observed in animal models (mice and rats), as well as in normal humans and in type I or type II diabetic patients. Accordingly, better understanding of how GLP-1R agonists modulate the activity of the HPA axis in diabetic subjects, especially obese individuals, will be crucial to design new and more efficient therapies for these patients.

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Section: Hpa In Diabetesmentioning

confidence: 99%

Stressing diabetes? The hidden links between insulinotropic peptides and the HPA axis

Diz-Chaves

Gil‐Lozano

Toba

et al. 2016

Journal of Endocrinology

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“…Disrupted control of adrenocorticotropic hormone (ACTH) release from pituitary corticotrophs and direct stimulation of corticotropin-releasing hormone of the adrenal gland with or without the release of ACTH leads to hyperactivation of the HPA in patients with diabetes [85]. Furthermore, the impairment of glucocorticoid-negative feedback sensitivity in patients with diabetes also results in increased activity of the HPA axis: following glucocorticoid administration, these patients exhibit a greater incidence of nonsuppression of pituitary-adrenal activity compared with non-diabetic individuals (43% vs 7%, respectively; p<0.01) [86]. Studies in STZ-treated rats have also shown that the basal hyperactivation of the HPA axis is associated with further decreased responsiveness of the HPA axis to stress, for example, to insulin-induced hypoglycaemia.…”

Section: Endocrinological Factorsmentioning

confidence: 99%

Type 1 diabetes mellitus and major depressive disorder: evidence for a biological link

et al. 2011

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Aims/hypothesis A growing body of research suggests that the prevalence of major depressive disorder (MDD) in children and youth with type 1 diabetes mellitus is significantly higher than that of youth without type 1 diabetes and is associated with increased illness severity. The objective of this article is to review the current literature on the pathophysiology of these two common diseases with respect to potential areas of overlapping biological dysfunction. Methods A search of English language articles published between 1966 and 2010 was conducted and augmented with manual review of reference lists from the identified publications. Results The evidence suggests plausible mechanisms whereby a biological relationship between type 1 diabetes and MDD may exist. These include the effects of circulating cytokines associated with autoimmune diabetes, the direct impact of insulin deficiency on neurogenesis/neurotransmitter metabolism, the effects of the chronic hyperglycaemic state, occurrence of iatrogenic hypoglycaemia and the impact of basal hyperactivity of the hypothalamic-pituitary-adrenal axis. Major depressive disorder (MDD) is highly prevalent among children and adolescents with type 1 diabetes mellitus. The prevalence of MDD among youth with type 1 diabetes (20-27%) is at least two to three times greater than the 5-8% background rate of MDD reported for non-diabetic youth [1, 2]. Early-onset MDD is severe, and in combination with diabetes (the third most common chronic disease in childhood), is associated with poorer diabetes control, increased Conclusions/interpretation

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“…In particular, some studies reported in these subjects an elevation of ACTH (10,12), basal (9 -11) and after dexamethasone test serum cortisol (13,14), and late-night salivary cortisol levels (15). In contrast, other previous studies (16 -17) did not show any alteration of pituitary-adrenal axis secretion.…”

Section: Diabetes Care 30:83-88 2007mentioning

confidence: 99%

Cortisol Secretion in Patients With Type 2 Diabetes

et al. 2007

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OBJECTIVE -The presence of an enhanced cortisol secretion in patients with type 2 diabetes is debated. In type 2 diabetic subjects, cortisol secretion was found to be associated with the complications and metabolic control of diabetes. We evaluated cortisol secretion in 170 type 2 diabetic subjects and in 71 sex-, age-, and BMI-matched nondiabetic subjects. RESEARCH DESIGN AND METHODS-In all subjects, we evaluated ACTH at 8:00 A.M. in basal conditions and serum cortisol levels at 12:00 P.M. (F24) and at 9:00 A.M. after a 1-mg overnight dexamethasone suppression test and 24-h urinary free cortisol (UFC). In diabetic patients, we evaluated the presence of chronic complications (incipient nephropathy, asymptomatic neuropathy, background retinopathy, and silent macroangiopathy). Patients were subdivided according to the absence (group 1, n ϭ 53) or presence (group 2, n ϭ 117) of diabetes complications.RESULTS -In group 2, UFC (125.2 Ϯ 4.6 nmol/24 h) and F24 (120.6 Ϯ 4.1 nmol/l) were higher than in group 1 (109.2 Ϯ 6.8 nmol/24 h, P ϭ 0.057, and 99.7 Ϯ 6.1 nmol/l, P ϭ 0.005, respectively) and in nondiabetic patients (101.7 Ϯ 5.9 nmol/24 h, P ϭ 0.002, and 100.3 Ϯ 5.3 nmol/l, P ϭ 0.003, respectively). In diabetic patients, the number of complications was associated with F24 (R ϭ 0.345; P Ͻ 0.0001) and diabetes duration (R ϭ 0.39; P Ͻ 0.0001). Logistic regression analysis showed that the presence of diabetes complications was significantly associated with F24, sex, duration of diabetes, and glycated hemoglobin.CONCLUSIONS -In type 2 diabetic subjects, hypothalmic-pituitary-adrenal activity is enhanced in patients with diabetes complications and the degree of cortisol secretion is related to the presence and number of diabetes complications. Diabetes Care 30:83-88, 2007I n patients with type 2 diabetes, glucocorticoid secretion has been suggested to be a possible link between insulin resistance and the features of the metabolic syndrome (hypertension, obesity, coronary heart disease, hyperlipidemia, and type 2 diabetes) (1-4). In fact, while glucocorticoid excess (overt or subclinical) has been demonstrated to lead to diabetes or to worsen metabolic control (5-7), the relationship between cortisol levels, insulin resistance, and chronic complications in type 2 diabetic patients without hypercortisolism is still a matter of debate.In past years, the hypothalamicpituitary-adrenal (HPA) axis secretion in patients with type 2 diabetes has been extensively investigated (8 -14). In particular, some studies reported in these subjects an elevation of ACTH (10,12), basal (9 -11) and after dexamethasone test serum cortisol (13,14), and late-night salivary cortisol levels (15). In contrast, other previous studies (16 -17) did not show any alteration of pituitary-adrenal axis secretion. The presence of chronic complications of type 2 diabetes (i.e., macroangiopathy, retinopathy, and neuropathy) has been associated to with HPA axis activity (9,18 -23), and an association between the degree of severity of several clinical measures of d...

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Abnormal Results of Dexamethasone Suppression Tests in Nondepressed Patients With Diabetes Mellitus

Cited by 95 publications

References 19 publications

Stressing diabetes? The hidden links between insulinotropic peptides and the HPA axis

Stressing diabetes? The hidden links between insulinotropic peptides and the HPA axis

Type 1 diabetes mellitus and major depressive disorder: evidence for a biological link

Cortisol Secretion in Patients With Type 2 Diabetes

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