The DOI matches its Crossref record; 43 of the 44 references it cites were found in a registry or an index.
Chronic streptozotocin diabetes in rats facilitates the acute stress response without altering pituitary or adrenal responsiveness to secretagogues.
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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“Elevated plasma glucagon and corticosterone levels are implicated in the pathogenesis of hyperglycemia in uDM (29 -31).”
From Leptin Activates a Novel CNS Mechanism for Insulin-Independent Normalization of Severe Diabetic Hyperglycemia (2011) · cites this paper as [31]
Citations
Cites
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Regulation of ACTH Secretion: Variations on a Theme of B
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Abnormal Hypothalamic–Pituitary–Adrenal Function in Anorexia Nervosa
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Corticosterone: narrow range required for normal body and thymus weight and ACTH
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Metadata
- Authors
- SCRIBNER, K. A., WALKER, C.-D., CASCIO, C. S., & DALLMAN, M. F.
- Affiliations
- University of California, San Francisco (US)
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- 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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