The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.
Neural dysregulation of peripheral insulin action and blood pressure by brain endoplasmic reticulum stress
Open accessAbstract
Chronic endoplasmic reticulum (ER) stress was recently revealed to affect hypothalamic neuroendocrine pathways that regulate feeding and body weight. However, it remains unexplored whether brain ER stress could use a neural route to rapidly cause the peripheral disorders that underlie the development of type 2 diabetes (T2D) and the metabolic syndrome. Using a pharmacologic model that delivered ER stress inducer thapsigargin into the brain, this study demonstrated that a short-term brain ER stress over 3 d was sufficient to induce glucose intolerance, systemic and hepatic insulin resistance, and blood pressure (BP) increase. The collection of these changes was accompanied by elevated sympathetic tone and prevented by sympathetic suppression. Molecular studies revealed that acute induction of metabolic disorders via brain ER stress was abrogated by NF-κB inhibition in the hypothalamus. Therapeutic experiments further revealed that acute inhibition of brain ER stress with tauroursodeoxycholic acid (TUDCA) partially reversed obesity-associated metabolic and blood pressure disorders. In conclusion, ER stress in the brain represents a mediator of the sympathetic disorders that underlie the development of insulin resistance syndrome and T2D.
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Cites
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Cited by
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Metadata
- Authors
- Purkayastha, S., Zhang, H., Zhang, G., Ahmed, Z., Wang, Y., & Cai, D.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2011-01-31
- Volume
- 108
- Issue
- 7
- Pages
- 2939-2944
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2144920399
- Cited by
- 179
- References
- 15
- FWCI
- 8.03
- Type
- journal article
- Language
- en
- Open access
- green
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