MECHANISM OF PROTECTION FROM ALLOXAN DIABETES PROVIDED BY NORMAL-BUTANOL

  • 1 January 1977
    • journal article
    • research article
    • Vol. 201  (2) , 450-455
Abstract
Pretreatment with n-butanol (10 mmol/kg i.p.) 30 min before alloxan (100 mg/kg) protects mice from the permanent hyperglycemic effects (measured at 72 h) of the diabetogenic agent. This dose of n-butanol caused an elevation of serum glucose at 30 min, the time of alloxan administration. Since glucose administration can protect animals from alloxan, the possibility that alcohol-induced hyperglycemia protected mice from alloxan was investigated. Mannoheptulose, an antagonist of glucose action at the pancreatic .beta.-cell, when given 24 min after n-butanol and 6 min before alloxan, eliminated the alcohol-induced protection. Fasted mice did not exhibit n-butanol-induced hyperglycemia at 30 min and alloxan given at that time produced diabetes. No protection was observed in fed animals when n-butanol was given 5 min before alloxan. The high serum levels of butanol and normal serum glucose which were observed at 5 min after alcohol administration indicated that the lack of protection was not due to a lack of circulating alcohol but resulted from an absence of hyperglycemia. Pretreatment with n-butanol appears to protect mice from alloxan-induced diabetes by the indirect mechanism of producing hyperglycemia at the time of alloxan administration.

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