Results from a 5-year study suggest that beta-cell function decline in patients with impaired fasting glucose/impaired glucose tolerance and type 2 diabetes is significantly worse than previously thought. Data also suggest that homeostasis model assessment of beta-cell function could markedly underestimate this decline, according to researchers.
The Insulin Resistance Atherosclerosis Study compared longitudinal changes in the beta-cell function of 1,052 patients according to their baseline glucose tolerance status (IFG/IGT; n=341), normal glucose tolerance (NGT; n=547) and patients newly diagnosed with type 2 diabetes (n=164).
“Despite this spectrum of evidence documenting the importance of beta-cell dysfunction in diabetes etiology, only limited data are available regarding longitudinal changes in beta-cell function, both overall and across glucose tolerance status categories,” the researchers wrote.
They used frequently sampled IV glucose tolerance tests to measure insulin secretion and insulin resistance and compared acute insulin response with the homeostasis model assessment of beta-cell function (HOMA B). Adjustments for underlying insulin resistance were made, according to researchers.
Patients with a glucose status of NGT and IFG/IGT displayed increased insulin secretion by as much as 30%, whereas those with type 2 diabetes showed a decline or insignificant changes to beta-cell function, according to data. However, decline in beta-cell function was significantly underestimated after adjustments for covariates using HOMA B for NGT (31%) vs. acute insulin response for IFG/IGT (50%) and using HOMA B for diabetes (70%) vs. acute insulin response for diabetes (80%).
These findings are clinically relevant based on a demand for interventions to prevent, delay or treat diabetes, researchers wrote.
Disclosure: Festa is employed by Eli Lilly and Company. All other researchers report no relevant financial disclosures.