The Finnish Diabetes Risk Score is associated with insulin resistance but not reduced ?-cell function, by classical and model-based estimates

Methods In this population-based cohort from the Hoorn municipal registry, subjects received an oral glucose tolerance test and a meal tolerance test on separate days, in random order, within 2 weeks. One hundred and eighty-six subjects, age 4166 years, with no known Type 2 diabetes were included. Of those, 163 (87.6%) had normal glucose metabolism and 23 (12.4%) had abnormal glucose metabolism(19 with impaired glucose metabolism; four with newly diagnosed Type 2 diabetes based on study results). Insulin sensitivity and beta-cell function (classical: insulinogenic index; ratio of areas under insulin/glucose curves; model-based: glucose sensitivity; rate sensitivity; potentiation) estimates were calculated from oral glucose tolerance test and meal tolerance test data.

Aims The Finnish Diabetes Risk Score (FINDRISC) is widely used for risk stratification in Type2 diabetes prevention programmes. Estimates of ?-cell function vary widely in people without diabetes and reduced insulin secretion has been described in people at risk for diabetes. The aim of this analysis was to evaluate FINDRISC as a tool to characterize reduced ?-cell function in individuals without known diabetes. Methods In this population-based cohort from the Hoorn municipal registry, subjects received an oral glucose tolerance test and a meal tolerance test on separate days, in random order, within 2weeks. One hundred and eighty-six subjects, age 41-66years, with no known Type2 diabetes were included. Of those, 163 (87.6%) had normal glucose metabolism and 23 (12.4%) had abnormal glucose metabolism (19 with impaired glucose metabolism; four with newly diagnosed Type2 diabetes based on study results). Insulin sensitivity and ?-cell function (classical: insulinogenic index; ratio of areas under insulin/glucose curves; model-based: glucose sensitivity; rate sensitivity; potentiation) estimates were calculated from oral glucose tolerance test and meal tolerance test data. Results FINDRISC was associated with insulin sensitivity (r=-0.41, P<0.0001), insulin/glucose areas under the curve (meal tolerance test: r=0.29, P<0.0001; oral glucose tolerance test: r=0.21, P=0.01) and potentiation factor (meal tolerance test: r=0.21, P=0.01). After adjusting for insulin sensitivity, these associations with ?-cell function were no longer significant. Conclusions After adjustment for insulin sensitivity, FINDRISC was not associated with reduced ?-cell function in subjects without known Type2 diabetes. While insulin secretion and insulin sensitivity are both components in Type2 diabetes development, insulin sensitivity appears to be the dominant component behind the association between FINDRISC and diabetes risk. © 2011 Merck Sharp & Dohme Corp.