Abstract
Background/objectiveThere is substantial interest in dietary approaches to reducing postprandial glucose (PPG) responses, but the quantitative contribution of PPG to longer-term glycemic control (reflected in glycated hemoglobin, HbA1c) in the general population is not known. This study quantified the associations of preprandial glucose exposure, PPG exposure, and glycemic variability with HbA1c and estimated the explained variance in HbA1c in individuals with and without type 2 diabetes (T2D).Subjects/methodsParticipants in the A1c-Derived Average Glucose (ADAG) study without T2D (n = 77) or with non-insulin-treated T2D and HbA1c<6.5% (T2DHbA1c < 6.5%, n = 63) or HbA1c ≥ 6.5% (T2DHbA1c ≥ 6.5%, n = 34) were included in this analysis. Indices of preprandial glucose, PPG, and glycemic variability were calculated from continuous glucose monitoring during four periods over 12 weeks prior to HbA1c measurement. In linear regression models, we estimated the associations of the glycemic exposures with HbA1c and calculated the proportion of variance in HbA1c explained by glycemic and non-glycemic factors (age, sex, body mass index, and ethnicity).ResultsThe factors in the analysis explained 35% of the variance in HbA1c in non-diabetic individuals, 49% in T2DHbA1c < 6.5%, and 78% in T2DHbA1c ≥ 6.5%. In non-diabetic individuals PPG exposure was associated with HbA1c in confounder-adjusted analyses (P < 0.05). In the T2DHbA1c < 6.5% group, all glycemic measures were associated with HbA1c (P < 0.05); preprandial glucose and PPG accounted for 14 and 18%, respectively, of the explained variation. In T2DHbA1c ≥ 6.5%, these glycemic exposures accounted for more than 50% of the variation in HbA1c and with equal relative contributions.ConclusionsAmong the glycemic exposures, PPG exposure was most strongly predictive of HbA1c in non-diabetic individuals, suggesting that interventions targeting lowering of the PPG response may be beneficial for long-term glycemic maintenance. In T2D, preprandial glucose and PPG exposure contributed equally to HbA1c.
Highlights
Hemoglobin A1c (HbA1c) reflects glycemic exposure in the previous 8–12 weeks[1]
In non-diabetic individuals postprandial glucose (PPG) exposure was associated with HbA1c in confounder-adjusted analyses (P < 0.05)
Among the glycemic exposures, PPG exposure was most strongly predictive of HbA1c in non-diabetic individuals, suggesting that interventions targeting lowering of the PPG response may be beneficial for long-term glycemic maintenance
Summary
Hemoglobin A1c (HbA1c) reflects glycemic exposure in the previous 8–12 weeks[1]. The level of HbA1c is in addition to glycemia determined by the lifespan of erythrocytes, which is affected by nutritional deficiencies, for Nutrition and DiabetesFærch et al Nutrition and Diabetes (2018)8:38 example, iron deficiency anemia and vitamin B12 deficiency[2]. Hemoglobin A1c (HbA1c) reflects glycemic exposure in the previous 8–12 weeks[1]. The level of HbA1c is in addition to glycemia determined by the lifespan of erythrocytes, which is affected by nutritional deficiencies, for Nutrition and Diabetes. In addition to nutritional deficiencies sex, genetic factors, and hematologic parameters are non-glycemic factors affecting HbA1c concentrations[1]. High HbA1c concentrations are associated with an increased risk for cardiovascular disease and mortality in individuals with and without type 2 diabetes (T2D)[3,4,5,6]. The exact contribution of normally experienced, daily PPG exposures and daytime glucose variability to variation in HbA1c in individuals with and without T2D is currently unknown, because few studies have captured these fluctuations over sustained periods under free-living conditions, for example, by use of continuous glucose monitoring (CGM)[8, 9]
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