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PRACTITIONERS SECTION
Year : 1997  |  Volume : 51  |  Issue : 4  |  Page : 128-129
 

Diabetes mellitus and glucokinase


Academy of Medical Sciences (ACME), Kannur-670 502, India

Correspondence Address:
K Ramachandran
Academy of Medical Sciences (ACME), Kannur-670 502
India
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PMID: 9355700

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How to cite this article:
Ramachandran K. Diabetes mellitus and glucokinase. Indian J Med Sci 1997;51:128-9

How to cite this URL:
Ramachandran K. Diabetes mellitus and glucokinase. Indian J Med Sci [serial online] 1997 [cited 2014 Jul 23];51:128-9. Available from: http://www.indianjmedsci.org/text.asp?1997/51/4/128/11541


Glucose uptake by cells is de­creased in diabetic state. Insulin is required for the uptake of glu­cose by Cells and the diabetic pa­tient lacks insulin or the patient has developed insulin resistance. Insulin resistance is due to an ab­normality in the insulin receptor. [1] In non insulin dependent diabetes mellitus (NIDDM) the principal de­fect is now attributed to the en­zyme glucokinase [2] for the develop­ment of this condition.

Hexokinases are the chief enzy­mes responsible for trappilng glu­cose into cells as Glucose - 6 - Phosphate (G6P). This enzyme exists in four isozyme forms and studies have shown that they are dimers of glucokinase. [3] Hexoki nase acts under normal fasting blood sugar levels and is respon­sible for glycolysis and energy supply. This enzyme is inhibited by product G6P. So all the glucose cannot be converted to G6P and thereby the metabolism of glucose is regulated. Once G6P is formed it cannot go out of the cell and has to undergo various fates depending on the tissue type or demand from the Cell.

In liver glucokinase is also pre­sent to bring out the conversion of glucose to G6P under hypergly­cemic conditions. This is not sub­jected to product inhibition by G6P and the enzyme is very active . [4] This is an additional advan­tage of liver cells to act as the principal organ for the metabolism of glucose or in converting extra glucose as glycogen. Now the occurrence of glucokinase in pan­creatic beta cells and in neuro­endocrine cells of the gastro intes­tinal tract is reported. [3] This en­zyme not only utilises glucose under hyperglycemia conditions but possesses an additional role as a- sensor or stimulator of insulin release from pancreatic beta cells. [2] Recent studies show that mutations in the gene of glucokinase enzyme has resulted in a decrease in the insulin released from the beta cells. [5][Additional file 1]

The cause of mutations in the gene of glucokinase is attributed to hereditary and environmental fac­tors. Maturity onset diabetes seen in young people (MODY) and ges­tational onset diabetes mellitus are all attributed to mutations in glucokinase gene. [6] Thus a key role is emerging for this enzyme in the development of various types of diabetes mellitus.

 
 ¤ References Top

1.Weir GC, Leahy JL. Pathogensis of NIDDM. In Joslin's Diabetes Mel­litus ed. CR. Kahn and GC Weir. 1994, 13th Ed. pp 240-81. Lea Febi­ger. Philadelphia.  Back to cited text no. 1      
2.Polonksy KS. The beta Cell in dia­betes from molecular genetics to clinical research. Diabetes 1995; 44:707-17.  Back to cited text no. 2      
3.Matschinsky FM. Glucokinase as glucose sensor and metabolic signal generator in pancreatic beta cells and hepatocytes. Diabetes. 1990; 33: 647-57.  Back to cited text no. 3      
4.Pilkis SJ, Granner DK. Moleucular Physiology of the regulation of hepatic gluconegenesis and glycoly­sis. Annual Review of Physiology, 1992;54:885-909.  Back to cited text no. 4      
5.Bell GJ, Pilkus SJ, Weber IT, Polonksy KS. Glucokinase muta­tions, Insulin Section and DM. Annual Review Physiology 1996;58: 171-187.  Back to cited text no. 5      
6.Zonali H, Vascillaire M, Lesage S, Sun F, Velho G. Linkage analysis and molecular scanning of gluco­kinase gene in NIDDM families. Diabetes, 1993;42:1238-45.  Back to cited text no. 6      




 

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