My biochemistry textbook says that "insulin increases glucose consumption that leads to elevation of G6P concentration".. But I'm failing to make a connection right here... Glucose consumption by what? by cells? Or is it about the glucose being absorbed in the glicolysis chain where glucokinase elevates G6P levels?

Insulin raises the amount of a particular class of GLUT transporter found on the plasma membrane of muscle and adipose tissues. I am not sure what you last sentence means.

base on my biochemistry book and my mind, insuline give impuls to the cell to elevate glucose intake from blood vessel. in the glicolysis phase, glucose will transform to G6P.it means insulin increases glucose consumption that leads to elevation of G6P concentration

One problem that we face in this type of question is that insulin increases the rates both of processes that lead to glucose 6-phosphate production and also of processes that lead to its consumption. The steady-state level of glucose 6-phosphate will be affected by both processes.

As far as I know glucokinase and hexokinase are not regulated by insulin per se. The main regulation of hexokinase is G6P, to inhibit overuse of the glycolytic pathway. GLUT4 on muscle and adipose surface is increased by insulin to take up the blood glucose, so this may be the means to increase glucose consumption and G6P production.

Insulin stimulates the rates of transcription of the genes for hexokinase II and hexokinase IV (also known as glucokinase). See table 15-5 in Nelson and Cox, Principles of Biochemistry, 6th edition.

Edited February 13, 20169 yr by BabcockHall

Quoting Wikipedia, "The amount of glucokinase can be increased by synthesis of new protein. Insulin is the principal signal for increased transcription, operating mainly by way of a transcription factor called sterol regulatory element binding protein-1c (SREBP1c) except in the liver. This occurs within an hour after a rise in insulin levels, as after a carbohydrate meal".

 

Insulin indeed increases G6P concentration by both increasing GLUT4 expression and glucokinase transcription.