Hello,

Following quote gives much informations about reasons to
hyperglycemia:-

"Role in Genetic Disorders
Many genetic disorders involve hereditary defects in receptor genes.
Often, it is hard to determine whether the receptor is nonfunctional or
the hormone is produced at decreased level; this gives rise to the
"pseudo-hypo-" group of endocrine disorders, where there appears to be
a decreased hormonal level while in fact it is the receptor that is not
responding sufficiently to the hormone.

[edit] Receptor Regulation
Cells can increase (upregulate) or decrease (downregulate) the number
of receptors to a given hormone or neurotransmitter to alter its
sensitivity to this molecule. This is a locally acting feedback
mechanism.

[edit] Mechanism
For insulin, the process of down regulation occurs when there are
elevated levels of the hormone in the blood. When insulin binds to its
receptors on the surface of a cell endocytosis of the hormone receptor
complex is initiated, only to be subsequently attacked by intracellular
lysosomal enzymes. The internalization is multi-purposed as it provides
the pathway for degradation of the hormone, and also a way to regulate
the number of sites that are available for binding on the cell’s
surface. At high plasma concentrations, the number of surface receptors
for insulin is gradually reduced by the accelerated rate of receptor
internalization and degradation brought about by increased hormonal
binding. The rate of synthesis of new receptors within the endoplasmic
reticulum and their insertion in the plasma membrane do not keep pace
with their rate of destruction. Over time, this self-induced loss of
target cell receptors for insulin reduces the target cell’s
sensitivity to the elevated hormone concentration. The process of
decreasing the number of receptor sites is virtually the same for all
hormones it only varies in the receptor hormone complex.

[edit] Cases
To illustrate this process we shall look at the insulin receptor sites
on the target cells of a Type II diabetic. Due to the elevated levels
of blood glucose from excessive feeding in an overweight individual the
β-cells (islets of Langerhans) in the pancreas must release more
insulin than normally emitted to match the demand and return the blood
to homeostatic levels. The near constant increase in blood insulin
levels results from an effort to match the increase in blood glucose
which will cause receptor sites on the person’s cell to down-regulate
and decrease the number of receptors for insulin, increasing the
subject’s resistance by decreasing sensitivity to this hormone. There
is also a hepatic decrease in sensitivity to insulin. This can be seen
in the continuing gluconeogenesis in the liver even when blood glucose
levels are elevated. This is the more common process of insulin
resistance, which in turn leads to a case of adult onset diabetes in
that subject. Other cases include Diabetes insipidus; here the kidneys
become insensitive to arginine vasopressin.

[edit] Reversal
There are ways to counteract this process; using the previous example a
Type II diabetic may increase their sensitivity to insulin through
proper diet and regular exercise producing weight loss, some may even
return to their pre-diabetic state following this
regimen.http://en.wikipedia.org/wiki/Receptor_%28biochemistry%29 "

It looks, primarily two reasons are indicated;

"the receptors are nonfunctional or the hormone is produced at
decreased level"

In case of diabetes, above may be relavent to type1(IDDM) and
type2(NIDDM). As such,

Whether the prime reason to getting hyperglycemia is that
hormone(insulin) is produced at decreased level in type1 and IDDM cases
whereas receptors are nonfunctional or lesser functional?

Other indicated reason to getting hyperglycemia is;

"There is also a hepatic decrease in sensitivity to insulin. This can
be seen in the continuing gluconeogenesis in the liver even when blood
glucose levels are elevated. This is the more common process of insulin
resistance, which in turn leads to a case of adult onset diabetes in
that subject."

I think it is also related to downgrade of receptors regulations.

How inflammatory cytokines produced by VAT, AGEs, fats senstive to
oxidations, infections etc. and decresed transcapillary movement of
insulin is to be related with above considerations?

Best wishes.