Abstract
Data regarding hyperglycemia-related factors were scarce in people without diabetes. Fifty males (age 50–65 years) with overweight/obesity but without diagnosis of diabetes were recruited. After excluding participants with the 2 h plasma glucose value during a 75 g oral glucose tolerance test ≥200 mg/dL, continuous glucose monitoring (CGM) was performed for 6 days. Subjects with ≥1800 CGM readings were included (n = 36). The CGM indices of hyperglycemia were significantly associated with disposition index and snacking frequency. In receiver-operating characteristic analysis for predicting the maximal CGM glucose ≥200 mg/dL, the area under curves of disposition index, snacking frequency, and minimal daily step counts during the study were 0.69, 0.63, and 0.68, whereas the cutoff values were 1.57, once daily, and 2499 steps, respectively. After adjustments, the lower disposition index (≤1.57), higher snacking frequency (≥1 per day), and lower minimal step (≤2499 steps per day) categories conferred 14.5, 14.5, and 6.6-fold increased probabilities for having the maximum level ≥ 200 mg/dL, respectively. In addition, the snacking habits were significantly associated with insulin resistance and compensatory hyperinsulinemia. In conclusion, in middle aged males with overweight/obesity but without diabetes, snacking and physical inactivity serve as the major drivers of postprandial hyperglycemia independently of β-cell function.
Highlights
Obesity and insulin resistance are major risk factors for type 2 diabetes [1]
Since the present study aims to test the prespecified hypotheses that certain specific lifestyle factors are related to the frequency of hidden hyperglycemia, the significant differences found in the study are not from the post hoc comparison but from the a priori planned comparisons
In this study, among men with overweight/obesity but without diabetes, 100% and 47% of the participants exhibited the maximal continuous glucose monitoring (CGM) glucose levels ≥140 mg/dL and ≥200 mg/dL, respectively, indicating that postprandial hyperglycemia prevails among non-diabetes
Summary
Obesity and insulin resistance are major risk factors for type 2 diabetes [1]. When the adaptive response of β-cells to increased insulin resistance is insufficient, hyperglycemia develops [2], which, along with other cytotoxic factors, further diminishes β-cell mass and function possibly through β-cell apoptosis [3]. By the time that type 2 diabetes is diagnosed, 50–80% of β-cell function is lost [1,4] and there is a significant reduction (24–65%) in β-cell mass [3,5], efforts for the prevention of β-cell dysfunction should be undertaken before the onset of diabetes. It is suggested that the onset of β-cell dysfunction may commence many years before the diagnosis of the disease [6]. The time point at which this abnormality begins and the factors that may be responsible for this pathological and functional change have not been elucidated [7].
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