Data/hora: 16/06/2024 07:44:30

Provedor de dados: | 60
País: | Brazil
Título: | Oral lactate intensifies insulin toxicity during severe insulin-induced hypoglycemia in mice
Autores: | Vilela,Vanessa Rodrigues; Antunes,Marina Masetto; Godoi,Vilma Aparecida Ferreira; Travassos,Patricia Batista; Souza,Helenir Medri de; Bazotte,Roberto Barbosa.
Data: | 2018-01-01
Ano: | 2018
Palavras-chave: | Lactatemia; Oral glucose; Diazepam; Seizure; Anticonvulsant effect.
Resumo: | ABSTRACT We investigated whether oral lactate could prevent seizures and deaths in mice with severe hypoglycemia induced by a high dose of insulin. For this purpose, mice were fasted for 15 h and then given an intraperitoneal injection of regular insulin (5.0 U/kg or 10.0 U/kg). Immediately after insulin injection, the mice received an oral dose of saline (control), glucose (5.5 mmol/kg), or lactate (18.0 mmol/kg). Glucose and lactate levels were measured in the blood and brain before and after the seizures began. Glucose and lactate delayed (p &lt; 0.05) the onset of seizures associated with severe insulin-induced hypoglycemia. Elevated (p &lt; 0.05) brain levels of lactate were associated with an absence of seizures in mice that received glucose or lactate, suggesting that lactate could prevent convulsions associated with severe insulin-induced hypoglycemia. However, the same oral dose of lactate that delayed the onset of convulsions also increased the mortality rate. In contrast, diazepam (3.0 mg/kg) prevented seizures and markedly decreased the frequency of death during severe insulin-induced hypoglycemia. The results demonstrated that in contrast to oral glucose, oral lactate intensifies insulin toxicity.
Tipo: | Info:eu-repo/semantics/article
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1984-82502018000200602
Editor: | Universidade de São Paulo, Faculdade de Ciências Farmacêuticas
Relação: | 10.1590/s2175-97902018000217617
Formato: | text/html
Fonte: | Brazilian Journal of Pharmaceutical Sciences  v.54 n.2 2018
Fonte: | info:eu-repo/semantics/openAccess