Reducing postprandial glucose in dietary intervention studies and the magnitude of the effect on diabetes-related risk factors: a systematic review and meta-analysis

Abstract

Purpose Reducing postprandial hyperglycemia has beneficial effects on diabetes-related risk factors, but the magnitude of the reduction needed to achieve such an effect is unknown. The purpose of the study was to quantify the relationship of acute glucose and insulin postprandial responses with longer-term effects on diabetes-related risk factors by performing a systematic review and meta-analysis of dietary intervention studies. Methods We systematically searched EMBASE and MEDLINE. Dietary intervention studies among any human population aiming to reduce postprandial glycemia, with actual measures of postprandial glucose (PPG) and/or insulin (PPI) as acute exposures (incremental area under the curve, iAUC) as well as markers of glucose metabolism (fasting glucose, HbA1c) and insulin sensitivity (fasting insulin, HOMA-IR) after at least 4 weeks of diet intervention as outcomes were included. Metaanalyses were performed for the effects on acute exposures and on diabetes-related risk factors. The relationship between changes in acute exposures and changes in risk factor outcomes was estimated by meta-regression analyses. Results Out of the 13,004 screened papers, 13 papers with 14 comparisons were included in the quantitative analysis. The dietary interventions acutely reduced mean PPG [mean difference (MD), − 0.27 mmol/l; 95% CI − 0.41 to − 0.14], but not mean PPI (MD − 7.47 pmol/l; 95% CI − 16.79 to 1.86). There were no significant overall effects on fasting glucose and insulin. HbA1c was reduced by − 0.20% (95% CI − 0.35 to − 0.05). Changes in acute PPG were significantly associated with changes in fasting plasma glucose (FPG) [per 10% change in PPG: β = 0.085 (95% CI 0.003, 0.167), k = 14], but not with fasting insulin [β = 1.20 (95% CI − 0.32, 2.71), k = 12]. Changes in acute PPI were not associated with changes in FPG [per 10% change in PPI: β = − 0.017 (95% CI − 0.056, 0.022), k = 11]. Conclusions Only a limited number of postprandial glucose-lowering dietary intervention studies measured acute postprandial exposures to PPG/PPI during the interventions. In this small heterogeneous set of studies, an association was found between the magnitude of the acute postprandial responses and the change in fasting glucose, but no other outcomes. More studies are needed to quantify the relationship between acute postprandial changes and long-term effects on risk factors.

Nutritional strategies to attenuate postprandial glycemic response

“…20,21 In addition to this, it is also very difficult to tease out the effects of postprandial glucose per se, because it is accompanied by elevated fasting blood glucose concentrations, and postprandial hyperlipidemia and hyperinsulinemia. 22 Especially the magnitude of the reduction in acute postprandial glucose exposure needed to achieve long-term metabolic health effects is currently unknown. A recent systematic review and meta-analysis of dietary intervention studies in relation to postprandial hyperglycemia showed that only a small heterogeneous set of dietary intervention studies are available where postprandial glucose was measured, and that more dietary intervention studies are needed.…”

“…A recent systematic review and meta-analysis of dietary intervention studies in relation to postprandial hyperglycemia showed that only a small heterogeneous set of dietary intervention studies are available where postprandial glucose was measured, and that more dietary intervention studies are needed. 22 Additionally, the authors of a recent systematic review and meta-analysis describing the effects of α-glucosidase-inhibiting drugs on acute postprandial glucose and insulin responses, were able to quantify clinically relevant estimates for a reduction in postprandial glucose per se, also for individuals without diabetes. 5 This meta-analysis indicates that a relative reduction of acute incremental postprandial glucose of ±45-50% (0.5 mmol/L in people without diabetes and 1.5 mmol/L in people with diabetes) can be seen as a clinically relevant reference point for reducing postprandial glucose concentrations via pharmaceutical and lifestyle interventions in the long term.…”

“…Furthermore, the number of participants used to test the GI of specific food items is often limited, and epidemiological nutritional studies estimate long‐term intakes for individual participants by using dietary questionnaires which are not optimally designed and also not validated for dietary GI and GL 20,21 . In addition to this, it is also very difficult to tease out the effects of postprandial glucose per se, because it is accompanied by elevated fasting blood glucose concentrations, and postprandial hyperlipidemia and hyperinsulinemia 22 . Especially the magnitude of the reduction in acute postprandial glucose exposure needed to achieve long‐term metabolic health effects is currently unknown.…”

“…Especially the magnitude of the reduction in acute postprandial glucose exposure needed to achieve long‐term metabolic health effects is currently unknown. A recent systematic review and meta‐analysis of dietary intervention studies in relation to postprandial hyperglycemia showed that only a small heterogeneous set of dietary intervention studies are available where postprandial glucose was measured, and that more dietary intervention studies are needed 22 . Additionally, the authors of a recent systematic review and meta‐analysis describing the effects of α‐glucosidase‐inhibiting drugs on acute postprandial glucose and insulin responses, were able to quantify clinically relevant estimates for a reduction in postprandial glucose per se, also for individuals without diabetes 5 .…”

Personalised Nutritional Recommendations Based on Individual Post-Prandial Glycaemic Responses Improve Glycaemic Metrics and PROMs in Patients with Type 2 Diabetes: A Real-World Assessment

“…The use of CGM in this group of patients was associated with improvements in glycaemic control that persisted in the long-term [ 11 ], weight loss, and improved diet [ 12 , 13 ]. Indeed, the effects of nutritional interventions on weight, HbA1c, and other lagging indicators of metabolic health and glycaemic control are well-explored, but there is much less understanding about the roles of very relevant and near-real-time indicators of metabolic health and glycaemic control on personalised dietary behaviour [ 19 ]. As CGM provides patients and their healthcare professionals with a large amount of data, guidelines have been created to standardise the analysis of PPGRs from CGM data, which rest on the identification of the maximum glucose level achieved after a meal, the difference between this maximum glucose and the value at meal start, and the time taken for the glucose to return to premeal levels [ 20 ].…”