Background:
@EN Glucokinase has been known as one of the key enzyme of glycolytic pathway. Recently, structure of glucokinase gene was identified and it was suspected as a glucose sensor of pancreas. Therefore defective in regulation of enzyme activity can
be
candidate for the cause of NIDDM. We have investigated the hypothesis that the pancreatic glucokinase ( PGK) is a glucose sensor and mediator of insulin secretion by examining the changes of PKG activity after the glucose load in diabetic
KK-mice.
@ES The animal model of NIDDM was induced with KK-mice by feeding them with high calorie diet for 4 months. After glucose load, liver and pancreas were collected from sacrificed animal and activities of gluco-kinase, hexokinase and
phosphofructokinase
were measured.
@EN Result:
@ES While PGK activity of normal control animals responded sensitivitely to the blood glucose level, the activity of the same enzyme in diabetic mice was significantly low and insensitive to the glucose load. The changes of hepatic glucokinase
(HGK)
during the glucose tolerance test period were linear increment up to 4 hors in both control and diabetic KK-mice. However the increment in diabetic animals was not so prominent. Phosphofructokinase, another key regulatory enzyme of glycolysis,
displayed
no difference in activity in both control and diabetic animals.
@EN Conclusion :
@ES These results indicate that the activities of PGK and HGK are regulated differently. PGF was affected by blood glucose level in normal mice, but improperly responded in diabetic animals. These data support the hypothesis that the pancreatic
glucokinase is a glucose sensor in mice.
@EN
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