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Download powerpoint Figure 2 Forest plot of controlled feeding trials investigating the effect of isocaloric exchange of fructose for other carbohydrate on A glycated blood proteins HbA1c and glycated albuminB fasting glucose, and C fasting insulin.
P values are for generic inverse variance random effects models. There were no studies investigating type 1 or undifferentiated diabetes for fasting insulin.
A high-quality color representation of this figure is available in the online issue. Patients had a median age of Their median baseline fasting glucose values were 9. The median follow-up was 4 weeks IQR 2— No hypercaloric feeding trials met the inclusion criteria.
A significant fasting glucose lowering effect was seen in the overall analysis after the systematic removal of either Bantle et al. There was no change in the interstudy heterogeneity during sensitivity analyses.
Meta-regression revealed no statistically significant subgroup effects Supplementary Fig. The median follow-up was 4 weeks IQR 3—10 weeks. No hypercaloric feeding trial met the inclusion criteria. Sensitivity analyses did not alter the effect estimate or degree of heterogeneity for fasting insulin, and meta-regression revealed no statistically significant subgroup effects Supplementary Fig.
None of the subjects were treated with insulin. Publication bias Supplementary Figs. CONCLUSIONS In Emerging standards of care final revision current aggregate analyses of 18 controlled feeding trials with subjects with type 1 and 2 diabetes, isocaloric fructose exchange for other carbohydrate decreased glycated blood proteins aggregated glycated albumin and HbA1c but not fasting glucose or insulin.
Food and Drug Administration for the development of new drugs for diabetes 29 and lies at the lower limit of efficacy expected for oral hypoglycemic agents The lack of change in fasting glucose and insulin suggests that fructose consumption does not promote hepatic and systemic insulin resistance.
Future meta-analyses of direct measures of insulin sensitivity would be of value. Our observed reduction in glycated blood proteins was consistent with the findings of an earlier meta-analysis by Livesey and Taylor 31who found an improvement in HbA1c It is important to note, however, that their analysis, in contrast to the current meta-analysis, did not focus exclusively on diabetes.
Unlike Livesey and Taylor 31we found the reduction in glycated blood proteins to be significant only in people with type 1 diabetes in stratified analyses. This discrepancy is likely due in part to the use of glycated albumin exclusively in the type 1 diabetes studies 15 The null finding in individuals with type 2 diabetes might be explained by the choice of glycated protein, because those trials used both HbA1c 9 — 1321 — 23 and glycated albumin 15 An improvement in glycemic control in individuals with type 2 diabetes is supported by an improvement in fasting glucose after removal of either Bantle et al.
It is noteworthy that the small, unusually precise study of Turner et al.
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Subgroup analyses revealed no significant effect modification for glycated blood proteins, fasting glucose, or insulin. Although Livesey and Taylor 31 in their earlier meta-analysis found that the improvement in HbA1c was dependent on the degree of dysglycemia, fructose dose, and follow-up, we did not find that these conditions altered any of the outcomes, nor in a separate analysis did we see any effect of fructose dose, follow-up, or comparator on triglycerides in type 2 diabetes with the same subgroup criteria There was, however, evidence of significant interstudy heterogeneity across most subgroup categories.
These may be related to real biological differences between study populations or to methodological differences between trials that were not assessed in our a priori subgroup analyses. A number of potential mechanisms have been proposed to explain the improvements in glycemia seen with the consumption of fructose.Proposed changes to federal public charge rule.
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