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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Lack of hepatic "interregulation" during inhibition of glycogenolysis in a canine model.

It has been proposed that the glycogenolytic and gluconeogenic pathways contributing to endogenous glucose production are interrelated. Thus a change in one source of glucose 6-phosphate might be compensated for by an inverse change in the other pathway. We therefore investigated the effects of 1,4-dideoxy-1,4-imino-D-arabinitol (DAB), a potent glycogen phosphorylase inhibitor, on glucose production in fasted conscious dogs. When dogs were treated acutely with high glucagon, glucose production rose from 1.93 +/- 0.14 to 3.07 +/- 0.37 mg x kg(-1) x min(-1) (P < 0.01). When dogs were treated acutely with DAB in addition to high glucagon infusion, the stimulation of the glycogenolytic rate was completely suppressed. Glucose production rose from 1.85 +/- 0.20 to 2.41 +/- 0.17 mg x kg(-1) x min(-1) (P < 0.05), which was due to the increase in gluconeogenesis from 0.93 +/- 0.09 to 1.54 +/- 0.08 mg x kg(-1) x min(-1) (P < 0.001). In conclusion, infusion of DAB inhibited glycogenolysis; however, the absolute contribution of gluconeogenesis to glucose production was not affected. These results suggest that inhibition of glycogenolysis could be an effective antidiabetic treatment.[1]

References

  1. Lack of hepatic "interregulation" during inhibition of glycogenolysis in a canine model. Fosgerau, K., Mittelman, S.D., Sunehag, A., Dea, M.K., Lundgren, K., Bergman, R.N. Am. J. Physiol. Endocrinol. Metab. (2001) [Pubmed]
 
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