Diabetes
This is what appears
to occur in diabetes.
In diabetes the balance
of hormone interplay is defective and blood glucose persistently remains above the normal range and complications arise.
Both type 1 and type
2 diabetes are caused by viruses that can establish latent and persistent infections: DNA viruses and retroviruses.
Type 1 diabetes
In type 1 diabetes
there is a diminished number of pancreatic B cells leading to the deficiency of insulin and other substances. The actions
of glucocorticoids, growth hormone, and other hormones are unopposed in absence of insulin. The number of insulin receptors
is not affected. However there is inadequate mobilization of insulin receptors, and consequently there is deficient production
of proteins necessary for the movement of glucose into the cells and for immune responses and this leads to metabolic and
non-metabolic complications.
The pancreatic A, B,
D, PP, and acini cells are derived from (like the intestinal epithelial cells from which they embryologically originated)
the same pleuripotent stem cells. In type 1 diabetes the B cells are not replenished because the committed precursor stem
cells do not proliferate and differentiate into mature B cells. It seems there is an excess of inhibitors and lack of growth
factors produced by the appropriate stromal cells. This is most likely due to a viral infection of stromal cells.
Type 2 diabetes
In type 2 diabetes
there is a persistent high blood glucose because of deficient insulin receptors. The insulin antagonists, which are normally
produced through growth hormone stimulation, are now autonomously produced by the liver as a result of a viral infection.
The proteins produced
through stimulation by insulin antagonists are also now made continuously and this leads to failure of movement sufficient
insulin receptors to the cell membrane and increased degradation of insulin receptors in the vesicles. Hence there is insulin
receptor deficiency. Glucocorticoids play a permissive role. The production of insulin receptors is not affected but does
not keep pace with the retention and degradation of insulin receptors.
The movement of insulin-sensitive
glucose transporters (GLUT 4) to the cell membrane and production of proteins necessary for immune response depend on stimulation
of adequate insulin receptors. Therefore there is compensatory increased insulin secretion to stimulate the few insulin receptors:
insulin resistance.
Complications of diabetes
The amount of insulin
and the number of insulin receptors required to stimulate the recycling of insulin-sensitive glucose transporters (GLUT 4)
are less than those required for the production of protein necessary for immune responses. There are therefore immune defects
of macrophages and neutrophils in type 1 and 2 diabetes. This leads to infections (non-metabolic complications) by certain
microorganisms. Viruses, most likely, cause small and large blood vessel diseases, nerve diseases, and hypertension. Bacteria
cause tuberculosis and skin, ear, and urinary tract infections. Fungi cause skin, and ear infections.
The metabolic complications,
like diabetic ketoacidosis, are due to hormonal imbalance.
The impotence common
in diabetics is probably due to over-activity of the thyroid gland leading to increased release of 3-iodotyrosine which may
inhibit sexual functions in the brain.
Treatment of diabetes
Based on these theories,
diabetes mellitus can now be treated resulting in the regression of the disease and complications. New treatment strategies
have emerged.
NB. We
wish to acknowledge and thank individuals and business houses that have donated generously to the research fund.
