Stress Drivers of Glucose Dynamics during Ozone Exposure Measured Using Radiotelemetry in Rats
Journal Article
·
· Environmental Health Perspectives
- U.S. Environmental Protection Agency (U.S. EPA), Research Triangle Park, NC (United States); Environmental Health Science and Research Bureau, Ottawa, ON (Canada)
- U.S. EPA, Research Triangle Park, NC (United States); ICF International Inc., Durham, NC (United States)
- U.S. Environmental Protection Agency (U.S. EPA), Research Triangle Park, NC (United States)
- National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC (United States)
- U.S. EPA, Research Triangle Park, NC (United States)
Inhaled irritant air pollutants may trigger stress-related metabolic dysfunction associated with altered circulating adrenal-derived hormones. We used implantable telemetry in rats to assess real-time changes in circulating glucose during and after exposure to ozone and mechanistically linked responses to neuroendocrine stress hormones. First, using a cross-over design, we monitored glucose during ozone exposures (0.0, 0.2, 0.4, and 0.8 ppm) and nonexposure periods in male Wistar Kyoto rats implanted with glucose telemeters. A second cohort of unimplanted rats was exposed to ozone (0.0, 0.4 or 0.8 ppm) for 30 min, 1 h, 2 h, or 4 h with hormones measured immediately post exposure. We assessed glucose metabolism in sham and adrenalectomized rats, with or without supplementation of adrenergic/glucocorticoid receptor agonists, and in a separate cohort, antagonists. Ozone (0.8 ppm) was associated with significantly higher blood glucose and lower core body temperature beginning 90 min into exposure, with reversal of effects 4–6 h post exposure. Glucose monitoring during four daily 4-h ozone exposures revealed duration of glucose increases, adaptation, and diurnal variations. Ozone-induced glucose changes were preceded by higher levels of adrenocorticotropic hormone, corticosterone, and epinephrine but lower levels of thyroid-stimulating hormone, prolactin, and luteinizing hormones. Higher glucose and glucose intolerance were inhibited in rats that were adrenalectomized or treated with adrenergic plus glucocorticoid receptor antagonists but exacerbated by agonists. We demonstrated the temporality of neuroendocrine-stress–mediated biological sequalae responsible for ozone-induced glucose metabolic dysfunction and mechanism in a rodent model.
- Research Organization:
- Oak Ridge Institute for Science and Education (ORISE), Oak Ridge, TN (United States)
- Sponsoring Organization:
- USDOE Office of Science (SC)
- Grant/Contract Number:
- SC0014664
- OSTI ID:
- 2425808
- Journal Information:
- Environmental Health Perspectives, Journal Name: Environmental Health Perspectives Journal Issue: 12 Vol. 130; ISSN 0091-6765
- Publisher:
- National Institute of Environmental Health SciencesCopyright Statement
- Country of Publication:
- United States
- Language:
- English
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