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Basal insulin sensitivity and beta cell function were calculated from fasting plasma glucose and insulin using HOMA [15].
OGTT-based indices of beta cell function were calculated.
In contrast, significant differences in indices of pancreatic beta cell function were found.
Basal hepatic glucose output, hepatic and peripheral insulin sensitivity and beta cell function were measured.
Thereafter, carbohydrates were added to the diet, and variables of beta cell function were monitored for 16 days.
Insulin resistance and beta cell function were predicted using the HOMA2 [ 29], and the area under the glucose curve (AUGC) was calculated using the trapezoidal rule [ 30].
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It is highly striking to observe that most of these TF and regulatory genes, which are likely to be functionally relevant for Ras-MAPK signaling and/or beta cell function, are overexpressed (Additional file 1: Table S1).
We know that beta cell function is adversely affected by glucose toxicity even with these mild glucose elevations [6].
Since beta cell function is affected by the concentration of glucose at the start of the test, the study protocol requested that no mixed meal test should be performed if fasting blood glucose was outside 4 11 mmol/l.
Beta cell function was increased (%B mean 225%, SD 88%, range 87%–348%), while insulin sensitivity was decreased (%S mean 46%, SD 52%, range 14% 198%) resulting in an increased insulin resistance (HOMA IR mean 3.7, SD 2.1, range 0.5 to 7.0).
Partial preservation of residual beta cell function is considered as clinically relevant goal also in the absence of lower insulin requirements, because of a lower risk of complications [20], [21].
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