Effects of Repetitive Hypoglycemia on Neuroendocrine Response and Brain Tyrosine Hydroxylase Activity in the Rat
| Autor: | P. Gronbeck, van Gertjan Dijk, Aryana Zavosh, Dianne P. Figlewicz, Charles W. Wilkinson, M. Higgins |
|---|---|
| Přispěvatelé: | Van Dijk lab |
| Rok vydání: | 2002 |
| Předmět: |
Male
Antimetabolites Antineoplastic medicine.medical_specialty STRESS Tyrosine 3-Monooxygenase VENTROMEDIAL HYPOTHALAMUS Physiology DEPENDENT DIABETES-MELLITUS Hypoglycemia Carbohydrate metabolism UNAWARENESS Glucagon Behavioral Neuroscience chemistry.chemical_compound Catecholamines Stress Physiological Corticosterone Internal medicine medicine Animals Rats Wistar Pure autonomic failure Glucocorticoids CORTICOSTERONE GENE-EXPRESSION RELEASE PARAVENTRICULAR NUCLEUS COUNTERREGULATION Tyrosine hydroxylase Endocrine and Autonomic Systems Brain INTENSIVE INSULIN THERAPY medicine.disease Neurosecretory Systems Rats Psychiatry and Mental health Glucose Neuropsychology and Physiological Psychology Endocrinology chemistry Neuroglucopenia Hypothalamus Brainstem Psychology |
| Zdroj: | Stress, 5(3), 217-226. Taylor & Francis Group |
| ISSN: | 1607-8888 1025-3890 |
| Popis: | Hypoglycemia-associated autonomic failure (HAAF) is a syndrome of acute adaptation to a metabolic stressor, in which neuroendocrine responses to repetitive hypoglycemic bouts are blunted. The CNS mechanisms that contribute to HAAF are unknown. In the present study, we modeled HAAF in the rat and measured the activity of tyrosine hydroxylase (TH) as an index of acute noradrenergic activation, to test the hypothesis that noradrenergic activation of the hypothalamus might be impaired. In association with a significant counter-regulatory response to a single bout of hypoglycemia (elevated corticosterone, catecholamines, and glucagon), TH activity was elevated overall in brainstem NE cell body areas and hypothalamus. With multiple hypoglycemic episodes in a 24 h period, the counter-regulatory response was blunted, and hypothalamic TH activity was comparable to that of saline-infused controls. In a similar paradigm, multiple bouts of CNS neuroglucopenia did not blunt the hyperglycemic or corticosterone responses, and were required for elevation of TH activity. This alternate response pattern suggests that insulin-induced hypoglycemia and cerebral neuroglucopenia represent somewhat different metabolic stressors at the CNS. |
| Databáze: | OpenAIRE |
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