Search

Background Noncommunicable disease development is related to impairments in glycemic and insulinemic responses, which can be modulated by fiber intake. Fiber's beneficial effects upon metabolic health can be partially attributed to the production of SCFAs via microbial fermentation of fiber in the gastrointestinal tract. Objectives We aimed to determine the effects of SCFAs, acetate, propionate, and butyrate on glycemic control in humans. Methods The CENTRAL, Embase, PubMed, Scopus, and Web of Science databases were searched from inception to 7 December 2021. Papers were included if they reported a randomized controlled trial measuring glucose and/or insulin compared to a placebo in adults. Studies were categorized by the type of SCFA and intervention duration. Random-effects meta-analyses were performed for glucose and insulin for those subject categories with ≥3 studies, or a narrative review was performed. Results We identified 43 eligible papers, with 46 studies within those records (n  = 913), and 44 studies were included in the meta-analysis. Vinegar intake decreased the acute glucose response [standard mean difference (SMD), −0.53; 95% CI, −0.92 to −0.14; n  = 67] in individuals with impaired glucose tolerance or type 2 diabetes and in healthy volunteers (SMD, −0.27; 95% CI, −0.54 to 0.00; n  = 186). The meta-analyses for acute acetate, as well as acute and chronic propionate studies, showed no significant effect. Conclusions Vinegar decreased the glucose response acutely in healthy and metabolically unhealthy individuals. Acetate, propionate, butyrate, and mixed SCFAs had no effect on blood glucose and insulin in humans. Significant heterogeneity, risks of bias, and publication biases were identified in several study categories, including the acute vinegar glucose response. As evidence was very uncertain, caution is urged when interpreting these results. Further high-quality research is required to determine the effects of SCFAs on glycemic control. [ABSTRACT FROM AUTHOR]

Obesity and type 2 diabetes (T2D) are increasingly common worldwide. While these disorders have increased in prevalence over the past several decades, there has been a concomitant reduction in sleep duration. Short sleep duration has been associated with higher rates of obesity and T2D, and the causality of these associations and their directionality, continue to necessitate evaluation. In this review we consider the evidence that sleep is an intrinsic factor in the development of obesity and chronic metabolic disorders, such as insulin resistance and T2D, while evaluating a potential bi-directional association. We consider the evidence that diet and meal composition, which are known to impact glycemic control, may have both chronic and acute impact upon sleep. Moreover, we consider that postprandial nocturnal metabolism and peripheral glycemia may affect sleep quality. We propose putative mechanisms whereby acute effects of nighttime glucose excursions may lead to increased sleep fragmentation. We conclude that dietary manipulations, particularly with respect to carbohydrate quality, may confer sleep benefits. Future research may seek to evaluate the effectiveness of synergistic nutrient strategies to promote sleep quality, with particular attention to carbohydrate quality, quantity, and availability as well as carbohydrate to protein ratio. [ABSTRACT FROM AUTHOR]