Adrenal Function and the Complications of Diabetes Mellitus

Lentle, Brian C.; Thomas, J. Hywel

doi:10.1016/s0140-6736(64)90616-6

Cited by 63 publications

(27 citation statements)

References 43 publications

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“…We have found that 72 hr-alloxinated rats showed higher levels of plasma corticosterone and an increase in the adrenal gland/body weight ratio, confirming previous reports (Lentle & Thomas 1964, Wexler & Lutmer 1975, Cameron et al 1987, Fitzpatrick et al 1992. These alterations in diabetes may probably be dependent on changes in the steroid feedback controlling mechanisms in the hypothalamicpituitary-adrenocortical system.…”

Section: Discussionsupporting

confidence: 90%

Antigen-induced pleural eosinophilia is suppressed in diabetic rats: role of corticosteroid hormones

Diaz¹,

Serra²,

Barreto³

et al. 1997

Mem. Inst. Oswaldo Cruz

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Section: Discussionsupporting

confidence: 90%

Antigen-induced pleural eosinophilia is suppressed in diabetic rats: role of corticosteroid hormones

Diaz¹,

Serra²,

Barreto³

et al. 1997

Mem. Inst. Oswaldo Cruz

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“…In atypical depression, frequent sampling of ACTH and cortisol revealed a dissociation of the hormone profiles that occurred periodically within days (80). A dissociation also occurred in patients with diabetes mellitus; mild chronic hypercortisolism in diabetic patients was accompanied by a diminished ACTH response to metyrapone (81).…”

Section: Does Non-acth-mediated Regulation Of the Adrenal Cortex Playmentioning

confidence: 98%

Adrenocorticotropin (ACTH)- and Non-ACTH-Mediated Regulation of the Adrenal Cortex: Neural and Immune Inputs

Bornstein

Chrousos

1999

The Journal of Clinical Endocrinology & Metabolism

276

121

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The maintenance of life depends on the capacity of the body to sustain its steady state or homeostasis; hence, the survival of the organism relies on its ability to react and adapt to the constant bombardment by physical and emotional threats or stressors (1, 2). To accomplish this, all living beings have developed an efficient but complex adaptive response system that allows the integration of the necessary defense mechanisms directed against both external and internal stressors. This coordinated response, the stress response, involves the nervous, endocrine, and immune systems. A qualitatively and quantitatively appropriate and time-limited stress response is a prerequisite for a healthy life. Inappropriate or inappropriately excessive and chronic hyperactivation of the stress system may lead to disease and, eventually, premature death.The two major peripheral limbs of the stress system are the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (1, 2). Their central components are, respectively, located in the hypothalamus and the brain stem. Stress-induced activation of the HPA axis is associated with release of hypothalamic CRH and vasopressin (AVP), the principal regulators of anterior pituitary corticotropin (ACTH) secretion, into the hypophyseal portal system. These hormones synergistically stimulate systemic ACTH secretion, which, in turn, stimulates the adrenal cortexes to secrete glucocorticoids. Central activation of the sympathetic neurons leads to activation of both the systemic sympathetic nervous system and, through the splanchnic nerves, the adrenal medullae (3). As the proper functioning of both the HPA axis and the sympathetic nervous system is crucial for survival and maintenance of health, it is not surprising that their regulation is developmentally plastic and complex, multilevel, and redundant. The regulation and central interaction of the HPA axis and the sympathetic nervous system and the immune system have been extensively studied and summarized in recent review articles (1, 3-5). The purpose of this brief review is to outline and discuss recent advances in the interactions and regulation of the adjacent peripheral limbs of the stress system, particularly the adrenal cortex and medulla, and to point out their implications for clinical endocrinology (Fig. 1).The adrenal gland has an astonishing capacity to adapt to various forms of acute and chronic stress (6 -8). After central activation of the HPA axis, ACTH triggers a physiologic, molecular, and morphological response of the adrenal cortex. This leads not only to glucocorticoid release, but also to up-regulation of steroidogenic cytochrome P 450 messenger ribonucleic acids (9, 10) and to conspicuous structural changes in the adrenal gland characterized by both hypervascularization and cellular hypertrophy and hyperplasia (11,12). These morphological changes are mirrored on the ultrastructural level; adrenocortical cells increase the number of their mitochondria, whereas their inner membranes form a dense vesi...

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“…Cortisol secretion is elevated in acidotic juvenile diabetics [9] and in patients with diabetic retinopathy and neuropathy [24], Such eleva tions, however, may be stress induced, since cortisol con centrations are reported to be in the normal range in diabet ics without acidosis or the above-noted complications. Un treated diabetic rats also evidence elevated plasma corticos terone concentrations, an increased adrenocortical re sponse to exogenous ACTH, and hypertrophied adrenal glands [6,23].…”

mentioning

confidence: 99%

Streptozotocin-Induced Diabetes Is Associated with Reduced Immunoreactive Beta-Endorphin Concentrations in Neurointermediate Pituitary Lobe and with Disrupted Circadian Periodicity of Plasma Corticosterone Levels

1985

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Lower concentrations of immunoreactive (IR) β-endorphin were present in the neurointermediate pituitary lobes of streptozotocin-induced diabetic versus control animals at both 2 and 4 weeks after the onset of diabetes. The forms of β-endorphin-like material present appeared to be similar in both groups when studied with cation-exchange chromatography. Insulin therapy via minipump for 2 weeks did not alter this finding of lowered β-endorphin concentrations in diabetic animals, despite normalization of blood glucose levels and body weight gain. Lower IR β-endorphin levels were also found in neurointermediate lobes of weight-restricted rats, but this group had increased plasma IR β-endorphin concentrations compared to diabetic animals. Concentrations of IR β-endorphin in microdissected brain regions and in anterior pituitaries of the diabetic animals failed to show consistent changes; in addition, ACTH concentrations in pituitary lobes and plasma did not differ among groups. Circadian rhythmicity of plasma insulin and corticosterone concentrations was absent in the diabetic animals, although food and water intake, while elevated, showed the normal nocturnal pattern of increased ingestion. Furthermore, adrenal hypertrophy was present in the diabetic animals and was accompanied by an elevation of mean plasma corticosterone levels. The present findings indicate that diabetes is associated with a decrease of neurointermediate pituitary lobe synthesis of β-endorphin, while not affecting the processing of the peptide in this lobe, and confirm previous reports of altered adrenal function in diabetic animals.

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Adrenal Function and the Complications of Diabetes Mellitus

Cited by 63 publications

References 43 publications

Antigen-induced pleural eosinophilia is suppressed in diabetic rats: role of corticosteroid hormones

Antigen-induced pleural eosinophilia is suppressed in diabetic rats: role of corticosteroid hormones

Adrenocorticotropin (ACTH)- and Non-ACTH-Mediated Regulation of the Adrenal Cortex: Neural and Immune Inputs

Streptozotocin-Induced Diabetes Is Associated with Reduced Immunoreactive Beta-Endorphin Concentrations in Neurointermediate Pituitary Lobe and with Disrupted Circadian Periodicity of Plasma Corticosterone Levels

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