The high blood glucose is related to the lack of GLUT receptor trans-location to the cell membrane to take up glucose, so I guess the glucose concentration is low. I am not sure about the second question.

High glucose concentration and insulin resistance are not the same, although both coincide in certain moments.

The concentration inside the cells is regulated by glucose trasporters, anf this depends on which cell are you asking for. For example Glut-2 (beta cell) is a high capacity low affinity glucose transporter and the concentarion inside the beta cell should be the same that outside. In the muscle is Glut-4... etc

Insulin is needed to incorporate glucose inside certain cells (muscle, adipose tissue) but not others (neurons)

Dear Bernat Soria 

Thank you for your answer. Yes I agree hyperglycemia can be due to relative absence of insulin (Type I DM).  My question is about type 2 DM patient characterized by  hyperglycemia (in plasma); what is the status inside cells ? high or low glucose  conc.  

which cell type?

Dear Bernat Soria 

My question is for all kind of cells. 

I think not all kinds of cells respond to the actions of insulin in the same way. Glucose uptake into cells is also driven by different transporters, some insulin sensitive, some others not so. take the brain, ..you may find insulin receptors in the brain, but the brain tissue can take up glucose with the low km glucose transporters like GLUT1 and 3 without influence from insulin. Muscle cells and adipose tissue need insulin.  In my opinion, in DM patients, there may be elevated level of glucose, and in the face of insulin resistance, or deficiency ,,, this intracellular glucose will be processed in to toxic metabolites (ROS, AGEs).... and contribute to cellular damage. ... the way I see it, in the absence of insulin signalling, IC glucose is as toxic, if not more due to the several kinds of enzymes that can transform glucose into AGEs .. .. 

Dear Jemal 

Thank you for your answer.

The primary  therapeutic goal for DM patients is to dispose (reduce) plasma glucose. Eg. one of the MoA of metformin is increases insulin dependent cellular up take of glucose (mainly to skeletal muscle).  If there is high conc. of glucose inside  cells,  would it not be more toxic then.  In fact, the toxic effect may be more pronounced in the plasma.

Glucose uptake and mobilization into addipose tissue and sk muscle cells depends on glucose transporters that are sensitive to insuline. Drugs like metformin enhance surface expression of GLUT4 (via a phosphorylative mechanism if i remember correctly). Going back to the original view point, DM patients are likely to have poor mobilzation of blood sugar into the storage sites,,skeletal muscle, adipose tissue (where glucose is stored as glycogen, or used o synthesize fat)

very few types of cells in which intracellular glucose concentration is equal to that of extracellular compartment, i.e. liver and islet B-cells of the pancreas. this is depending on the the type of glucose transporter in theses cells which allows, bidirectional movement of glucose. Other cells , particularly muscle and adipocytes, owing to the need to GLUT-4 to allow glucose entery, and this transporter is insulin-dependent, and is affected by intracellular signalling pathways that is regulated by autophosphorylation of many signalling molecules and all are regulated by insulin. In insulin resistance, these mechanisms are interrupted so that glucose entery is lacking contributing for hyperglycemia. Energy fuel in these cells as derived from fatty acid and ketone body oxidation. 

Dear Derbew, As mentioned in few of the above comments, 'all cells do not respond the same way'. The skeletal muscle cells, adipocytes and hepatocytes have lesser glucose inside as the channel is insulin dependent. Whereas, few cells like retinal and brain cells are insulin independent in the uptake of glucose and will have relatively more glucose inside the cells, which manifests as diabetes complications (via polyol pathway). 

 The above mentioned answer is a more conventional apporach. If you wish to think a little out of the box and explore further on the patho-physiology invlolved DM, please read through the following links, which might give you some directions. 

All the very best!

http://www.sciencedirect.com/science/article/pii/S0014579398011491

http://nadeem.no/2012/10/07/glucose-uptake-is-not-insulin-dependant/

http://advan.physiology.org/content/ajpadvan/38/4/308.full.pdf