Differences in the blood glucose response of mice to alloxan and alloxan-inhibiting compounds
Boquist, L.
Acta Endocrinologica 92(4): 687-693
1979
ISSN/ISBN: 0001-5598 PMID: 532524 Document Number: 150288
A typical triphasic blood glucose response (response A) is seen in fed and starved mice treated with alloxan alone, whereas a marked initial hyperglycemia (to which alloxan probably has not contributed) and an abolished second hyperglycemia (response B) are found in starved mice given D-glucose, D-fructose, D-mannose and sodium lactate, and in fed mice treated with p-hydroxymercuribenzoate (PMB), D-mannoheptulose (MH) or diphenylhydantoin (DPH) before alloxan injection. An abolished initial hyperglycemia, but a preserved 2nd hyperglycemia (response C), is observed in starved mice given PMB, MH or DPH before alloxan, indicating that an initial hyperglycemia is not a prerequisite for B-cell damage and development of alloxan diabetes. Fed and starved mice pretreated with NaHCO3, acetazolamide (AZM), L-Leu or tolbutamide exhibit neither any initial nor any 2nd hyperglycemia (response D) following alloxan injection. The inhibition of alloxan toxocity caused by pretreatment with D- glucose, D-fructose, D-mannose, PMB, MH or DPH, and to some extent also sodium lactate, is dependent upon development of hyperglycemia which may affect the B-cells secondarily and make them insensitive to alloxan, whereas these compounds are not antagonistic to alloxan in the absence of hyperglycemia, e.g., when PMB, MH or DPH are given to starved mice. NaHCO3, AZM, L-Leu and tolbutamide seem to antagonize alloxan by other mechanism(s), probably through a direct action upon the B-cells.