Diabetes mellitus and glucokinase

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

Diabetes mellitus and glucokinase

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

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

PMID: 9355700

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 2013 May 21];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

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.
2.	Polonksy KS. The beta Cell in diabetes from molecular genetics to clinical research. Diabetes 1995; 44:707-17.
3.	Matschinsky FM. Glucokinase as glucose sensor and metabolic signal generator in pancreatic beta cells and hepatocytes. Diabetes. 1990; 33: 647-57.
4.	Pilkis SJ, Granner DK. Moleucular Physiology of the regulation of hepatic gluconegenesis and glycolysis. Annual Review of Physiology, 1992;54:885-909.
5.	Bell GJ, Pilkus SJ, Weber IT, Polonksy KS. Glucokinase mutations, Insulin Section and DM. Annual Review Physiology 1996;58: 171-187.
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.

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