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

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

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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Crossref · 10.1210/endo-129-1-99

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Authors
SCRIBNER, K. A., WALKER, C.-D., CASCIO, C. S., & DALLMAN, M. F.
Affiliations
University of California, San Francisco (US)
Venue
Endocrinology
Published
1991-07
Volume
129
Issue
1
Pages
99-108
ISSN
  • 0013-7227 (ISSN-L)
  • 1945-7170
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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