β Cell Failure in Type 2 Diabetes Mellitus: Microvascular Pancreatic Isletopathy?
Abstract Number: 2316-PO
Authors: UDAYA M. KABADI.
Institutions: Phoenix, AZ; Iowa City, IA.
Results: UKPDS suggested relentless deterioration of β cell function as a part of natural course of type 2 diabetes mellitus (DM2). However, the course was apparently not universal since almost 25% of patients maintained glycemic goal (<7.0%) at 9 years while receiving oral agents. Moreover, the exact mechanism of progressive β cell failure is unclear. It is plausible that β cell failure may be due to microangiopathy of pancreatic islets since no organ or tissue is exempt from this complication. Therefore we examined the occurrence of β cell failure in 300 men with ages 40-75 years and duration of DM 4-23 years. Subjects were divided into 4 groups according to number of microvascular manifestations (MM) i.e., 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 intact (β +ve) with HbA1c <7.0% with diet and oral drugs. The results are shown below
Table 1% of patients are shown in parentheses; * - p <0.01 vs. group 0; † - p < 0.001 vs. group 0Prevalence of β cell failure was progressive with increasing numbers of microvascular manifestations. Therefore, the β cell failure may also be a manifestation of microvascular pancreatic isletopathy.
|No. of MM||0||1||2||3|
|β + ve||85 (65)||32 (34)*||5 (11)†||5 (16)†|
|β - ve||46 (35)||62 (66)*||39 (89)†||26 (84)†|
|Total||131 (100)||94 (100)||44 (100)||31 (100)|