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http://www.scirp.org/journal/PaperInformation.aspx?PaperID=53118#.VLXOUsnQrzE
Affiliation(s)
1University of Iowa Carver College of Medicine, Iowa City, Iowa, USA.
2VA Medical Center, Phoenix, Arizona, USA.
3Des Moines University, Des Moines, Iowa, USA.
2VA Medical Center, Phoenix, Arizona, USA.
3Des Moines University, Des Moines, Iowa, USA.
ABSTRACT
Background: UKPDS suggested relentless deterioration of β
cell function as a part of natural course of type 2 diabetes mellitus.
However, the course was apparently not universal since many patients
maintained glycemic goal (HbA1c < 7.0%) at 9 years while receiving
conventional life style programs consisting of diet and exercise or/and
oral agents. Moreover, β cell failure occurred around the same
time as the time of onset of microvascular complications. Finally, the
exact mechanism of progressive β cell failure remains to be defined. It is plausible that β
cell failure may be due to fibrosis of pancreatic islets secondary to
microangiopathy since no organ or tissue is exempt from this
complication. Objective: To assess epidemiologic correlation between
presence of b cell failure and microvascular complications by
determining the prevalence of β cell failure in subjects with
type 2 diabetes with increasing number of known microvascular
complications. Methods: 650 Subjects with ages 40-75 years and duration
of DM 4-23 years were divided into 4 groups according to number of
microvascular complications, e.g. retinopathy, nephropathy, and
neuropathy. β cell failure (β - ve ) is defined as
HbA1c > 7.0% with any therapy or HbA1c < 7.0% with insulin, either
monotherapy or in combination with oral agents. β cell function is deemed “preserved” (β
+ ve) with HbA1c < 7.0% with treatment consisting of life style
program or/and oral drugs. Results: Prevalence of b cell failure
progressively rose with increasing number of microvascular complications
from 0 to 2 with no further significant rise with 3 complications
whereas subjects with preserved β cell function declined with
increasing number of microvascular complications (p < 0.01 for both
groups). Significant relationships were also noted between the age and
the duration of diabetes and prevalence of β cell failure (p < 0.01). The relative risks rose progressively for β
cell failure/β cell preserved with increasing number of microvascular
complications as well as the greater duration of Diabetes. However, a
significantly (p < 0.01) higher relative risk for β cell
failure persisted for rising number of microvascular complications even
after eliminating the influence of age and duration of diabetes.
Conclusion: β cell failure may be a manifestation of microvascular pancreatic isletopathy similar to other microvascular complications.
Cite this paper
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