Why the study?
How do beta-endorphin, ACTH, and catecholamine levels respond to insulin-induced hypoglycemia in patients with chronic autonomic failure compared to normal subjects?
How do beta-endorphin, ACTH, and catecholamine levels respond to insulin-induced hypoglycemia in patients with chronic autonomic failure compared to normal subjects?
Peripheral adrenergic activity is not essential for beta-endorphin and ACTH release in humans, as demonstrated by normal responses in IOH but impaired responses in MSA.
Answers are grounded in this paper and cite their sources.
May aid differentiation of MSA from IOH; leaves open clinical relevance of blunted responses.
Plasma epinephrine (EPI), norepinephrine (NE), beta-endorphin, and corticotropin (ACTH) responses were measured during insulin-induced hypoglycemia in normal subjects and in patients with either multiple system atrophy (MSA) or idiopathic orthostatic hypotension (IOH). In normal subjects, there was a striking rise in EPI, NE, beta-endorphin, and ACTH following the nadir of hypoglycemia. Both beta-endorphin and ACTH responses were significantly lower than normal in patients with MSA, in contrast to normal levels in IOH patients. No correlation was observed between the degree of adrenergic insufficiency and the beta-endorphin and ACTH responses. The normal peptide responses in IOH are consistent with involvement limited to the peripheral sympathetic nervous system, whereas lesions in the central nervous system in MSA interfere with release of beta-endorphin and ACTH in response to hypoglycemia. The strong correlation between beta-endorphin and ACTH levels is consistent with their common origin. Peripheral adrenergic activity is not essential for beta-endorphin and ACTH release in humans.
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Polinsky et al. (1987) studied this question.
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