Cited by 112Stress Responses and CortisolAdrenal Hormones and DisordersNeuropeptides and Animal Physiology

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Chronic streptozotocin diabetes in rats facilitates the acute stress response without altering pituitary or adrenal responsiveness to secretagogues.

SCRIBNER, KAREN A., WALKER, CLAIRE-DOMINIQUE, CASCIO, CAREN S., DALLMAN, MARY F.·1991·Endocrinology

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Abstract

We have used streptozotocin (STZ)-induced diabetes in rats to determine whether this represents a sustained stimulus to the adrenocortical system and whether STZ-diabetic rats are able to mount an acute stress response. Furthermore, we compared pituitary responsiveness to CRF and/or arginine vasopressin, and adrenal responsiveness to ACTH in STZ- vs. vehicle-treated rats. We also compared the efficacy of dexamethasone inhibitory feedback in STZ-diabetic and control rats. Our results show that STZ-treated rats chronically hypersecrete corticosterone (B) as evidenced by their decreased thymus weights, their increased urinary B excretion, and their elevated mean plasma B levels during the light hours of the day. Despite the evidence for sustained hypersecretion of B, STZ-treated rats showed greater and more prolonged ACTH and B responses to the acute stress of histamine injection. However, when tested separately, neither pituitary nor adrenal responsiveness to their secretagogues were increased in STZ-diabetic compared to control rats. Dexamethasone inhibition of stress-induced B secretion was tested using two different paradigms: pentobarbital-anesthetized rats were given iv injections of acid saline, and awake rats were given ip injections of histamine. In both experiments the STZ-treated rats were relatively resistant to glucocorticoid inhibition of stress responses. This finding, taken together with the exaggerated ACTH and B responses to stress, strongly suggests that the facilitatory effects of chronic STZ-diabetes are a consequence of changes in sensitivity of central neural components of the adrenocortical system to stimulatory and/or inhibitory inputs, in conjunction with changes in glucocorticoid feedback sensitivity.

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Authors: SCRIBNER, K. A., WALKER, C.-D., CASCIO, C. S., & DALLMAN, M. F.
Affiliations: University of California, San Francisco (US)
ORCID: WALKER, CLAIRE-DOMINIQUE
Venue: Endocrinology
Publisher: The Endocrine Society
Published: 1991-07
Volume: 129
Issue: 1
Pages: 99-108
ISSN: 0013-7227 (ISSN-L)
1945-7170
DOI: 10.1210/endo-129-1-99
OpenAlex: W2124250661
Cited by: 112
References: 44
Citations by year: 2025: 1 · 2024: 1 · 2022: 2 · 2020: 1 · 2018: 2 · 2014: 3 · 2013: 1 · 2012: 1
FWCI: 2.57
Type: journal article
Language: en
Open access: closed
Locations: Endocrinology (publishedVersion)
PubMed (publishedVersion)
Funders: University of California, San Francisco
National Institute of Diabetes and Digestive and Kidney Diseases (DK28172)
Topics: Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
Keywords: streptozotocin-induced diabetes, chronic diabetes, acute stress response, corticosterone, ACTH secretion, pituitary responsiveness, vasopressin, corticotropin-releasing factor, glucocorticoid negative feedback, thymus weight, adrenal response
MeSH terms: Adrenal Glands, Adrenocorticotropic Hormone, Animals, Arginine Vasopressin, Circadian Rhythm, Corticosterone, Corticotropin-Releasing Hormone, Dexamethasone, Diabetes Mellitus, Experimental, Histamine, Male, Pituitary Gland, Rats, Inbred Strains, Stress, Physiological, Rats

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Chronic streptozotocin diabetes in rats facilitates the acute stress response without altering pituitary or adrenal responsiveness to secretagogues.

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