Key result
In patients with pancreatic diabetes, the presence of autonomic neuropathy was associated with a severely blunted adrenalin response to insulin-induced hypoglycemia (2.4-fold vs 19.0-fold increase, p<0.01).
Why the study?
Does diabetic autonomic neuropathy impair counterregulatory hormone responses to insulin-induced hypoglycemia in patients with pancreatic diabetes?
Observational (n=13)
No
Does diabetic autonomic neuropathy impair counterregulatory hormone responses to insulin-induced hypoglycemia in patients with pancreatic diabetes?
Patients with pancreatic diabetes and autonomic neuropathy have severely impaired adrenalin and glucagon responses to hypoglycemia, increasing their risk for severe hypoglycemic coma.
Answers are grounded in this paper and cite their sources.
May heighten severe hypoglycemia risk in pancreatic diabetes with neuropathy; hypothesis-generating for impaired counterregulation.
NAKAMURA, T., TAKEBE, K., KUDOH, K., ISHII, M., IMAMURA, K., KIKUCHI, H., KASAI, F., TANDOH, Y., YAMADA, N., ARAI, Y., TERADA, A. and MACHIDA, K. Decreased Counterregulatory Hormone Responses to Insulin-Induced Hypoglycemia in Patients with Pancreatic Diabetes Having Autonomic Neuropathy. Tohoku J. Exp. Med., 1994, 174 (4), 305-315 - Thrirteen patients with pancreatic diabetes caused by calcifying pancreatitis were divided into 2 groups; 5 with diabetic autonomic neuropathy [AN(+) group] and 8 without [AN(-) group]. They were subjected to an insulin-induced hypoglycemic stress test to evaluate their blood pancreatic glucagon, adrenalin, and cortisol responses. When a blood glucose level below 45mg/100ml was defined to be hypoglycemia, all the patients in the AN(-) group exhibited peripheral adrenalin responses, with a significant increase (mean, 19.0 times the basal level) in the blood adrenalin level. Among the AN(+) group, on the other hand, central nervous symptoms became evident rather than the peripheral adrenalin response (the blood adrenalin level hardly exceeded the basal level). With the exception of a single patient, none exhibited responses in the blood pancreatic glucagon levels. Only one patient showed a minimal cortisol response but the remaining 12 reacted normally in the cortisol release. The findings are summarized as follows: in pancreatic diabetes, insulin-induced hypoglycemia causes little change in pancreatic glucagon secretion; when the condition is complicated with autonomic neuropathy, central nervous symptoms develop while the blood adrenalin level hardly increases. These findings indicated that patients with pancreatic diabetes complicated with diabetic autonomic neuropathy have a risk of lapsing into an acute hypoglycemic coma and difficulty in recovering from the hypoglycemic state.
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Nakamura et al. (1994) conducted an observational in Pancreatic diabetes (n=13). Autonomic neuropathy vs. Without autonomic neuropathy was evaluated on Maximal incremental rate of blood adrenalin in response to insulin-induced hypoglycemia (p=<0.01). In patients with pancreatic diabetes, the presence of autonomic neuropathy was associated with a severely blunted adrenalin response to insulin-induced hypoglycemia (2.4-fold vs 19.0-fold increase, p<0.01).
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