Hypothalamic-pituitary-adrenal axis dysregulation among diabetic outpatients

Roy, Monique; Collier, Bronwyn; Roy, Alec

doi:10.1016/0165-1781(90)90106-f

Cited by 103 publications

(66 citation statements)

References 20 publications

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“…Second, the changes in endocrine systems caused by diabetes may affect the function of 5-HT 1A receptors. Type 1 and type 2 diabetes cause hyperactivation of the hypothalamic-pituitary-adrenal (HPA) axis in humans (Cameron et al, 1984;Roy et al, 1990Roy et al, , 1993 and animals (Scribner et al, 1991;Takao et al, 2000). In consistent with these previous reports, diabetic mice showed the increases in plasma corticosterone levels in our present result.…”

Section: Discussionsupporting

confidence: 83%

Diabetes Attenuates the Antidepressant-Like Effect Mediated by the Activation of 5-HT1A Receptor in the Mouse Tail Suspension Test

Miyata

Hirano

Kamei

2003

Neuropsychopharmacol

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Several lines of evidence have indicated that the prevalence of depression in diabetic subjects is higher than that in the general population, however, little information is available on the effects of antidepressants in diabetes. In the present study, the antidepressantlike effect mediated by the activation of 5-HT 1A receptors was examined using the tail suspension test in streptozotocin-induced diabetic mice. Long-lasting increases in 5-HT turnover rates were observed in the diabetic mouse midbrain and frontal cortex, but not in the hippocampus. Duration of immobility was significantly longer in diabetic than in nondiabetic mice in the tail suspension test. The 5-HT 1A receptor agonist ( 7 )-8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) (3-30 mg/kg, i.p.) reduced the duration of immobility in nondiabetic mice, and this effect was completely antagonized by pretreatment with, a selective 5-HT 1A receptor antagonist. In contrast, 8-OH-DPAT (3 mg/kg-3 mg/kg, i.p.) was ineffective in diabetic mice. The selective 5-HT reuptake inhibitor fluoxetine (3-56 mg/kg, i.p.) reduced the duration of immobility in both nondiabetic and diabetic mice. However, fluoxetine was less effective in diabetic mice than in nondiabetic mice. WAY-100635 (30 mg/kg, s.c.) reversed the suppression of the duration of immobility by fluoxetine (30 mg/kg, i.p.) in nondiabetic mice. On the other hand, the anti-immobility effect of fluoxetine (56 mg/kg, i.p.) was not antagonized by WAY-100635 (30 mg/kg, s.c.) in diabetic mice. The selective 5-HT 2 receptor antagonist 6-methyl-1-(1-methylethyl)-ergoline-8b-carboxylic acid 2-hydroxy-1-methylpropyl ester (LY53,857) (30 mg/kg, s.c.) reversed the anti-immobility effect of fluoxetine in both nondiabetic and diabetic mice. Spontaneous locomotor activity in diabetic mice was not different from that in nondiabetic mice. 8-OH-DPAT (30 mg/kg, i.p.), but not fluoxetine, increased the spontaneous locomotor activity in both nondiabetic and diabetic mice. The number of 5-HT 1A receptors in the mouse frontal cortex was unaffected by diabetes. Plasma corticosterone levels in diabetic mice were significantly higher than that in nondiabetic mice. These results suggest that the antidepressant-like effect mediated by 5-HT 1A receptors may be attenuated by diabetes.

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Section: Discussionsupporting

confidence: 83%

Diabetes Attenuates the Antidepressant-Like Effect Mediated by the Activation of 5-HT1A Receptor in the Mouse Tail Suspension Test

Miyata

Hirano

Kamei

2003

Neuropsychopharmacol

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“…Hyperactivity of the hypothalamic-pituitary-adrenal axis with consequent hypercortisolism was frequently observed in patients with type 1 and type 2 diabetes (Cameron et al 1984, Roy et al 1990, 1998, Chan et al 2002, and seemed to be associated with increased expression of hypothalamic corticotrophin-releasing hormone (CRH) mRNA (Chan et al 2003). We described an increase in the adrenal-gland/body weight rate in parallel to an elevation in serum corticosterone levels following diabetes caused by alloxan treatment in rats.…”

Section: Balance Between Steroid and Insulin Levels In Diabetesmentioning

confidence: 99%

Mast cell changes in experimental diabetes: focus on attenuation of allergic events

Carvalho

Barreto

Cordeiro

et al. 2005

Mem. Inst. Oswaldo Cruz

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“…Indeed, plasma ACTH and cortisol levels are elevated in patients with untreated diabetes mellitus, suggesting that hyperglycemia is a metabolic stress [1][2][3]. Animal experiments using a diabetic rat model support the observation as well [4][5][6].…”

Section: Introductionmentioning

confidence: 60%

“…Roy et al reported the increase in plasma ACTH and plasma and urinary cortisol in diabetic patients [1][2][3]. In vivo experiments using the type 2 diabetic rat model showed similar effects [4][5][6], and Schwartz et al found a decrease in hypothalamic CRH expression despite the increase in ACTH and cortisol, suggesting the existence of unknown factor(s) stimulating the HPA axis at the pituitary level during high blood glucose [5].…”

Section: Discussionmentioning

confidence: 95%

High glucose activates pituitary proopiomelanocortin gene expression: possible role of free radical‐sensitive transcription factors

Asaba

Iwasaki

Asai

et al. 2006

Diabetes Metabolism Res

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Hypothalamic-pituitary-adrenal axis dysregulation among diabetic outpatients

Cited by 103 publications

References 20 publications

Diabetes Attenuates the Antidepressant-Like Effect Mediated by the Activation of 5-HT1A Receptor in the Mouse Tail Suspension Test

Diabetes Attenuates the Antidepressant-Like Effect Mediated by the Activation of 5-HT1A Receptor in the Mouse Tail Suspension Test

Mast cell changes in experimental diabetes: focus on attenuation of allergic events

High glucose activates pituitary proopiomelanocortin gene expression: possible role of free radical‐sensitive transcription factors

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