الفهرس 
Material and methodsOnly 14 pages are availabe for public view
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Abstract
Epidemiological evidence has led to the identification of a
consistent marker of cardiovascular risk in non diabetic populations,
i.e. Plasma insulin levels. Subjects with hyperinsulinemia and normal
blood glucose levels exhibit a state of resistance to insulin whether this
is as a cause or a consequence of hyperinsulinemia is still unresolved.
Experimental evidence ascribes to insulin resistance. Several
clinical and metabolic abnormalities usually mild, e. g elevated blood
pressure, a disturbed lipid profile, glucose intolerance. The most
natural biological marker of insulin resistance i.e. hyperinsulinemia as
an independent predictor of CHD mortality risk, supports the
hypothesis that a cluster of mild abnormalities can lead to significant
increased arterial damage.
This cluster of mild abnormalities is probably present long before a
susceptible patient develops frank hyperglycemia and eventually type II
diabetes. Indeed, type II diabetes appears to develop essentially in
individuals who suffer from syndrome X. This is evidenced by the fact
that high levels of insulinemia predict future type II diabetes in glucose
tolerant subjects. Type II diabetes has a strong hereditary component
and children who have one or both parents with type II diabetes are
susceptible for developing the disease later in life. At an early age,
although their glucose tolerance is normal, these children have some
degree of insulin resistance and significantly higher levels of plasma
insulin than age-matched children with no parental susceptibility to
diabetes.
This evidence suggest that the development of arterial damage or
conditions for cardiovascular complications, probably start long before
diabetes is diagnosed by chronic hyperglycemia.
Pancreas transplantation unlike heart or liver transplantation, is not
an immediate life saving procedure. The objective of a pancreas
transplantation is to improve the quality of life and to favorably
influence the secondary complications of diabetes that would otherwise
arise several years hence. Pancreas transplantation is similar to kidney
transplantation, in that if kidney fails the patient can resume dialysis.
Rejection, or other causes of pancreatic graft failure should be
followed by a return to exogenous insulin therapy and resumption of a
life style no different than that achieved pre transplant. Pancreatic
transplantation has contributed to the understanding of diabetes in
several respects, including defining its autoimmune nature. Many
other fundamental questions related to the nature of diabetes mellitus,
such as etiology or its association with microvascular and other
complications may also be forthcoming from observation of the
pancreas transplant recipients.
The mounting body of evidence suggest that pancreas
transplantation does confer benefits to the patient make it a worthwhile
procedure though the true benefits while not be known until long term
follow-up in clinical trials has been established in a significant number
of patients. Should islet cell transplantation become a realistic
alternative then whole organ pancreas transplantation will undoubtedly
become obsolete. Until then it remains the new gold standard against
which other treatments must be compared.
In conclusion, this canine model of hyperinsulinemia demonstrates
that elevated insulin levels may be associated with significant
disturbances in blood pressure, lipoprotein profile and atherosclerosis.
We can also implicate that portal-enteric transplantation of the
pancreas leads to lower insulin levels. Therefore, this approach may
be important for the prevention of atherosclerotic vascular disease in
transplant recipients.