Background Starchy foods can have a profound effect on metabolism. The structural properties of starchy foods can affect their digestibility and postprandial metabolic responses, which in the long term may be associated with the risk of type 2 diabetes and obesity. Objectives This systematic review sought to evaluate the clinical evidence regarding the impact of the microstructures within starchy foods on postprandial glucose and insulin responses alongside appetite regulation. Methods A systematic search was performed in the PUBMED, Ovid Medicine, EMBASE, and Google Scholar databases for data published up to 18 January 2021. Data were extracted by 3 independent reviewers from randomized crossover trials (RCTs) that investigated the effect of microstructural factors on postprandial glucose, insulin, appetite-regulating hormone responses, and subjective satiety scores in healthy participants. Results We identified 745 potential articles, and 25 RCTs (n = 369 participants) met our inclusion criteria: 6 evaluated the amylose-to-amylopectin ratio, 6 evaluated the degree of starch gelatinization, 2 evaluated the degree of starch retrogradation, 1 studied starch–protein interactions, and 12 investigated cell and tissue structures. Meta-analyses showed that significant reductions in postprandial glucose and insulin levels was caused by starch with a high amylose content [standardized mean difference (SMD) = −0.64 mmol/L*min (95% CI: −0.83 to −0.46) and SMD = −0.81 pmol/L*min (95% CI: −1.07 to −0.55), respectively], less-gelatinized starch [SMD = −0.54 mmol/L*min (95% CI: −0.75 to −0.34) and SMD = −0.48 pmol/L*min (95% CI: −0.75 to −0.21), respectively], retrograded starch (for glucose incremental AUC; SMD = −0.46 pmol/L*min; 95% CI: −0.80 to −0.12), and intact and large particles [SMD = −0.43 mmol/L*min (95% CI: −0.58 to −0.28) and SMD = −0.63 pmol/L*min (95% CI: −0.86 to −0.40), respectively]. All analyses showed minor or moderate heterogeneity (I2 < 50%). Sufficient evidence was not found to suggest how these structural factors influence appetite. Conclusions The manipulation of microstructures in starchy food may be an effective way to improve postprandial glycemia and insulinemia in the healthy population. The protocol for this systematic review and meta-analysis was registered in the international prospective register of systematic reviews (PROSPERO) as CRD42020190873.

Background Non-communicable disease development is related to impairments in glycaemic and insulinemic response, which can be modulated by fiber intake. Fiber's beneficial effect upon metabolic health can be partially attributed to the production of short-chain fatty acids (SCFAs) via microbial fermentation of fiber in the gastrointestinal tract. Objective We aimed to determine the effect of the SCFAs, acetate, propionate, and butyrate on glycemic control in humans. Methods CENTRAL, Embase, PubMed, Scopus and Web of Science databases were searched from inception to the 07/12/2021. 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), 44 studies were included in the meta-analysis. Vinegar intake decreased acute glucose response, standard mean difference (SMD) and (95% CI) –0.53 (–0.92, –0.14) (n = 67) in individuals with impaired glucose tolerance or type 2 diabetes and in healthy (SMD) –0.27 (–0.54, 0.00) (n = 186). The meta-analyses for acute acetate as well as acute and chronic propionate studies had no significant effect. Conclusions Vinegar decreased glucose response acutely in healthy and non-healthy. Acetate, propionate, butyrate, and mixed SCFAs had no effect on blood glucose and insulin in humans. Significant heterogeneity, risk of bias, and publication bias were identified in several study categories, including 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 effect of SCFAs on glycemic control.

BackgroundType 2 diabetes (T2D) diagnoses are predicted to reach 643 million by 2030, increasing incidences of cardiovascular disease and other comorbidities. Rapidly digestible starch elevates postprandial glycemia and impinges glycemic homeostasis, elevating the risk of developing T2D. Starch can escape digestion by endogenous enzymes in the small intestine when protected by intact plant cell walls (resistant starch type 1), when there is a high concentration of amylose (resistant starch type 2) and when the molecule undergoes retrogradation (resistant starch type 3) or chemical modification (resistant starch type 4). Dietary interventions using resistant starch may improve glucose metabolism and insulin sensitivity. However, few studies have explored the differential effects of resistant starch type. This systematic review and meta-analysis aims to compare the effects of the resistant starch from intact plant cell structures (resistant starch type 1) and resistant starch from modified starch molecules (resistant starch types 2–5) on fasting and postprandial glycemia in subjects with T2D and prediabetes.MethodsDatabases (PubMed, SCOPUS, Ovid MEDLINE, Cochrane, and Web of Science) were systematically searched for randomized controlled trials. Standard mean difference (SMD) with 95% confidence intervals (CI) were determined using random-effects models. Sub-group analyses were conducted between subjects with T2D versus prediabetes and types of resistant starch.ResultsThe search identified 36 randomized controlled trials (n = 982), 31 of which could be included in the meta-analysis. Resistant starch type 1 and type 2 lowered acute postprandial blood glucose [SMD (95% CI) = -0.54 (–1.0, –0.07)] and [–0.96 (–1.61, –0.31)]. Resistant starch type 2 improved acute postprandial insulin response [–0.71 (–1.31, –0.11)]. In chronic studies, resistant starch type 1 and 2 lowered postprandial glucose [–0.38 (–0.73, –0.02), –0.29 (–0.53, –0.04), respectively] and resistant starch type 2 intake improved fasting glucose [–0.39 (–0.66, –0.13)] and insulin [–0.40 (–0.60, –0.21)].ConclusionResistant starch types 1 and 2 may influence glucose homeostasis via discrete mechanisms, as they appear to influence glycemia differently. Further research into resistant starch types 3, 4, and 5 is required to elucidate their effect on glucose metabolism. The addition of resistant starch as a dietary intervention for those with T2D or prediabetes may prevent further deterioration of glycemic control.