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Glucose and Fructose Hydrogel Enhances Running Performance, Exogenous Carbohydrate Oxidation, and Gastrointestinal Tolerance.
Rowe, JT, King, RFGJ, King, AJ, Morrison, DJ, Preston, T, Wilson, OJ, O'Hara, JP
Medicine and science in sports and exercise. 2022;(1):129-140
Abstract
PURPOSE Beneficial effects of carbohydrate (CHO) ingestion on exogenous CHO oxidation and endurance performance require a well-functioning gastrointestinal (GI) tract. However, GI complaints are common during endurance running. This study investigated the effect of a CHO solution-containing sodium alginate and pectin (hydrogel) on endurance running performance, exogenous and endogenous CHO oxidation, and GI symptoms. METHODS Eleven trained male runners, using a randomized, double-blind design, completed three 120-min steady-state runs at 68% V˙O2max, followed by a 5-km time-trial. Participants ingested 90 g·h-1 of 2:1 glucose-fructose (13C enriched) as a CHO hydrogel, a standard CHO solution (nonhydrogel), or a CHO-free placebo during the 120 min. Fat oxidation, total and exogenous CHO oxidation, plasma glucose oxidation, and endogenous glucose oxidation from liver and muscle glycogen were calculated using indirect calorimetry and isotope ratio mass spectrometry. GI symptoms were recorded throughout the trial. RESULTS Time-trial performance was 7.6% and 5.6% faster after hydrogel ([min:s] 19:29 ± 2:24, P < 0.001) and nonhydrogel (19:54 ± 2:23, P = 0.002), respectively, versus placebo (21:05 ± 2:34). Time-trial performance after hydrogel was 2.1% faster (P = 0.033) than nonhydrogel. Absolute and relative exogenous CHO oxidation was greater with hydrogel (68.6 ± 10.8 g, 31.9% ± 2.7%; P = 0.01) versus nonhydrogel (63.4 ± 8.1 g, 29.3% ± 2.0%; P = 0.003). Absolute and relative endogenous CHO oxidation was lower in both CHO conditions compared with placebo (P < 0.001), with no difference between CHO conditions. Absolute and relative liver glucose oxidation and muscle glycogen oxidation were not different between CHO conditions. Total GI symptoms were not different between hydrogel and placebo, but GI symptoms were higher in nonhydrogel compared with placebo and hydrogel (P < 0.001). CONCLUSION The ingestion of glucose and fructose in hydrogel form during running benefited endurance performance, exogenous CHO oxidation, and GI symptoms compared with a standard CHO solution.
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Effect of fructose instead of glucose or sucrose on cardiometabolic markers: a systematic review and meta-analysis of isoenergetic intervention trials.
Fattore, E, Botta, F, Bosetti, C
Nutrition reviews. 2021;(2):209-226
Abstract
CONTEXT Free, or added, sugars are considered important determinants in the pandemics of obesity and associated chronic diseases, and fructose has emerged as the sugar of main concern. OBJECTIVE The aim of this review was to assess the evidence of the effects of isoenergetic replacement of fructose or high-fructose corn syrup (HFCS) for glucose or sucrose on cardiometabolic markers in controlled dietary intervention trials. DATA SOURCES The electronic databases PubMed/MEDLINE, the Cochrane Library, and Embase were searched from 1980 to May 5, 2020. STUDY SELECTION Studies were eligible if they measured at least one of the following outcomes: total cholesterol, low- and high-density lipoprotein cholesterol, triacylglycerols, apolipoprotein A1, apolipoprotein B, systolic blood pressure, diastolic blood pressure, fasting glucose, and body weight. DATA EXTRACTION For each outcome, the mean values and the corresponding measure of dispersion were extracted after the intervention or control diet. DATA ANALYSIS Fixed-effects and random-effects models were used to pool study-specific estimates. Between-study heterogeneity was assessed by the χ2 test and the I2 statistic and publication bias by the Egger test and funnel plots. RESULTS Twenty-five studies involving 1744 volunteers were identified. No significant effects were found when fructose or HFCS was substituted for glucose, except for a slight decrease in diastolic blood pressure when fructose was substituted for glucose. Similarly, no effects were found when fructose or HFCS was substituted for sucrose, except for a small increase, of uncertain clinical significance, of apolipoprotein B when HFCS was substituted for sucrose. CONCLUSIONS Isoenergetic substitution of fructose or HFCS for glucose or sucrose has no significant effect on most of the cardiometabolic markers investigated; however, some results were affected by residual between-study heterogeneity and studies with high or unclear risk of bias. SYSTEMATIC REVIEW REGISTRATION PROSPERO registration number CRD42016042930.
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Dietary carbohydrates and fats in nonalcoholic fatty liver disease.
Yki-Järvinen, H, Luukkonen, PK, Hodson, L, Moore, JB
Nature reviews. Gastroenterology & hepatology. 2021;(11):770-786
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Abstract
The global prevalence of nonalcoholic fatty liver disease (NAFLD) has dramatically increased in parallel with the epidemic of obesity. Controversy has emerged around dietary guidelines recommending low-fat-high-carbohydrate diets and the roles of dietary macronutrients in the pathogenesis of metabolic disease. In this Review, the topical questions of whether and how dietary fats and carbohydrates, including free sugars, differentially influence the accumulation of liver fat (specifically, intrahepatic triglyceride (IHTG) content) are addressed. Focusing on evidence from humans, we examine data from stable isotope studies elucidating how macronutrients regulate IHTG synthesis and disposal, alter pools of bioactive lipids and influence insulin sensitivity. In addition, we review cross-sectional studies on dietary habits of patients with NAFLD and randomized controlled trials on the effects of altering dietary macronutrients on IHTG. Perhaps surprisingly, evidence to date shows no differential effects between free sugars, with both glucose and fructose increasing IHTG in the context of excess energy. Moreover, saturated fat raises IHTG more than polyunsaturated or monounsaturated fats, with adverse effects on insulin sensitivity, which are probably mediated in part by increased ceramide synthesis. Taken together, the data support the use of diets that have a reduced content of free sugars, refined carbohydrates and saturated fat in the treatment of NAFLD.
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Dietary fructose as a model to explore the influence of peripheral metabolism on brain function and plasticity.
Gomez-Pinilla, F, Cipolat, RP, Royes, LFF
Biochimica et biophysica acta. Molecular basis of disease. 2021;(5):166036
Abstract
High consumption of fructose has paralleled an explosion in metabolic disorders including obesity and type 2 diabetes. Even more problematic, sustained consumption of fructose is perceived as a threat for brain function and development of neurological disorders. The action of fructose on peripheral organs is an excellent model to understand how systemic physiology impacts the brain. Given the recognized action of fructose on liver metabolism, here we discuss mechanisms by which fructose can impact the brain by interacting with liver and other organs. The interaction between peripheral and central mechanisms is a suitable target to reduce the pathophysiological consequences of neurological disorders.
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Optimization of Initial Cation Concentrations for L-Lactic Acid Production from Fructose by Lactobacillus pentosus Cells.
Wang, J, Jiang, S, Huang, J, Guo, H, Bi, X, Hou, M, Chen, X, Hou, S, Lin, H, Lu, Y, et al
Applied biochemistry and biotechnology. 2021;(5):1496-1512
Abstract
In this study, Box-Behnken design was applied to optimize the initial concentrations of 4 cations for L-lactic acid production from fructose by homologous batch fermentation of Lactobacillus pentosus cells. The optimum initial cation concentrations were obtained as 6.542 mM Mg2+, 3.765 mM Mn2+, 2.397 mM Cu2+, and 3.912 mM Fe2+, respectively. The highest L-lactic acid yield and productivity were obtained as 0.935 ± 0.005 g/g fructose and 1.363 ± 0.021 g/(L × h), respectively, with a maximum biomass concentration of 7.97 ± 0.17 g/L. The effectiveness of the optimization by Box-Behnken design was confirmed based on the small errors between predicted results and experimental results shown as 0.3%, - 0.2%, and - 1.2%, respectively. The quadratic models with high accuracy and reliability can be applied to mathematically forecasted the fermentation performance. After the optimization, the lactic acid yield and productivity were significantly improved by 3.7% and 21.0%, respectively.
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Metabolic liver disease - what's in a name?
Herman, MA
Nature reviews. Endocrinology. 2021;(2):79-80
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Metabolic-Associated Fatty Liver Disease (MAFLD), Diabetes, and Cardiovascular Disease: Associations with Fructose Metabolism and Gut Microbiota.
Drożdż, K, Nabrdalik, K, Hajzler, W, Kwiendacz, H, Gumprecht, J, Lip, GYH
Nutrients. 2021;(1)
Abstract
Non-alcoholic fatty liver disease (NAFLD) is an increasingly common condition associated with type 2 diabetes (T2DM) and cardiovascular disease (CVD). Since systemic metabolic dysfunction underlies NAFLD, the current nomenclature has been revised, and the term metabolic-associated fatty liver disease (MAFLD) has been proposed. The new definition emphasizes the bidirectional relationships and increases awareness in looking for fatty liver disease among patients with T2DM and CVD or its risk factors, as well as looking for these diseases among patients with NAFLD. The most recommended treatment method of NAFLD is lifestyle changes, including dietary fructose limitation, although other treatment methods of NAFLD have recently emerged and are being studied. Given the focus on the liver-gut axis targeting, bacteria may also be a future aim of NAFLD treatment given the microbiome signatures discriminating healthy individuals from those with NAFLD. In this review article, we will provide an overview of the associations of fructose consumption, gut microbiota, diabetes, and CVD in patients with NAFLD.
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Acute administration of fructans increases the number of transient lower esophageal sphincter relaxations in healthy volunteers.
Geysen, H, Gielis, E, Deloose, E, Vanuytsel, T, Tack, J, Biesiekierski, JR, Pauwels, A
Neurogastroenterology and motility. 2020;(1):e13727
Abstract
INTRODUCTION Dietary measures are often advised to patients with gastro-esophageal reflux disease (GERD). Fermentable Oligo-, Di-, Mono-saccharides and Polyols (FODMAPs) induce lower gastrointestinal (GI) symptoms. However, their effects on esophageal motility, including transient lower esophageal sphincter relaxations (TLESRs), reflux events and GERD symptoms are unknown. We investigated the effect of acute administration of two FODMAPs, fructose, and fructans, on the number of TLESRs, reflux episodes and symptom perception in healthy volunteers (HVs). MATERIALS After an overnight fast, 20 HVs (10 males; 32.6 ± 2.8 years) underwent a high-resolution impedance manometry. The number of TLESRs and reflux episodes was quantified during five hours after consumption of a high-caloric meal (740 kcal) enriched with 40 g of either fructose, fructans or glucose (as placebo). Results were analyzed using mixed models. RESULTS There was a trend for a change in the number of TLESRs between the three conditions (P = .06). Post hoc analysis revealed a trend toward a higher number of TLESRs in the fructan condition compared with placebo (Pcorr = .06). Acute administration of fructose did not influence the number of TLESRs. The total number of reflux events was not affected by either FODMAP condition. Lower esophageal sphincter (LES) pressures dropped significantly in the first postprandial hour to recover slowly back to baseline values (P < .0001), without any difference in LES pressure between the three conditions. CONCLUSION Ingestion of fructans increased the number of TLESRs slightly compared with placebo. The effect of FODMAPs such as fructans or a low FODMAP diet on reflux parameters in GERD patients remains to be investigated.
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Effect of fructose and its epimers on postprandial carbohydrate metabolism: A systematic review and meta-analysis.
Braunstein, CR, Noronha, JC, Khan, TA, Mejia, SB, Wolever, TM, Josse, RG, Kendall, CW, Sievenpiper, JL
Clinical nutrition (Edinburgh, Scotland). 2020;(11):3308-3318
Abstract
AIMS: To synthesize the evidence of the effect of small doses (≤30-g/meal) of fructose and its epimers (allulose, tagatose, and sorbose) on the postprandial glucose and insulin response to carbohydrate-containing meals. METHODS MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials were searched through to April 9, 2019. We included randomized (RCTs) and non-randomized acute, single-meal, controlled feeding trials that added ≤30-g of fructose or its epimers either prior to or with a carbohydrate-containing meal compared with the same meal alone. Outcomes included the incremental area under the curve (iAUC) for glucose and insulin, the Matsuda Insulin Sensitivity Index, and the Early Insulin Secretion Index. Data were expressed as ratio of means (RoM) with 95% CIs and pooled using the inverse variance method. The overall certainty of the evidence was evaluated using GRADE. RESULTS Forty trial comparisons (n = 400) were included (none for sorbose). Allulose significantly reduced the postprandial iAUC glucose response by 10% (0.90 [0.84 to 0.96], P < 0.01). Tagatose significantly reduced the postprandial iAUC insulin response by 25% (0.75 [0.62 to 0.91], P < 0.01) and showed a non-significant 3% reduction in the postprandial iAUC glucose response (0.97 [0.94 to 1.00], P = 0.07). There was no effect of fructose on any outcome. The certainty of the evidence was graded as low to moderate for fructose, moderate for allulose, and low for tagatose. CONCLUSIONS Small doses of allulose and tagatose, but not fructose, lead to modest improvements on postprandial glucose and insulin regulation. There is a need for long-term RCTs to confirm the sustainability of these improvements.
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Synergistic effects of fructose and glucose on lipoprotein risk factors for cardiovascular disease in young adults.
Hieronimus, B, Medici, V, Bremer, AA, Lee, V, Nunez, MV, Sigala, DM, Keim, NL, Havel, PJ, Stanhope, KL
Metabolism: clinical and experimental. 2020;:154356
Abstract
BACKGROUND Fructose consumption increases risk factors for cardiometabolic disease. It is assumed that the effects of free sugars on risk factors are less potent because they contain less fructose. We compared the effects of consuming fructose, glucose or their combination, high fructose corn syrup (HFCS), on cardiometabolic risk factors. METHODS Adults (18-40 years; BMI 18-35 kg/m2) participated in a parallel, double-blinded dietary intervention during which beverages sweetened with aspartame, glucose (25% of energy requirements (ereq)), fructose or HFCS (25% and 17.5% ereq) were consumed for two weeks. Groups were matched for sex, baseline BMI and plasma lipid/lipoprotein concentrations. 24-h serial blood samples were collected at baseline and at the end of intervention. Primary outcomes were 24-h triglyceride AUC, LDL-cholesterol (C), and apolipoprotein (apo)B. Interactions between fructose and glucose were assessed post hoc. FINDINGS 145 subjects (26.0 ± 5.8 years; body mass index 25.0 ± 3.7 kg/m2) completed the study. As expected, the increase of 24-h triglycerides compared with aspartame was highest during fructose consumption (25%: 6.66 mmol/Lx24h 95% CI [1.90 to 11.63], P = 0.0013 versus aspartame), intermediate during HFCS consumption (25%: 4.68 mmol/Lx24h 95% CI [-0.18 to 9.55], P = 0.066 versus aspartame) and lowest during glucose consumption. In contrast, the increase of LDL-C was highest during HFCS consumption (25%: 0.46 mmol/L 95% CI [0.16 to 0.77], P = 0.0002 versus aspartame) and intermediate during fructose consumption (25%: 0.33 mmol/L 95% CI [0.03 to 0.63], P = 0.023 versus aspartame), as was the increase of apoB (HFCS-25%: 0.108 g/L 95%CI [0.032 to 0.184], P = 0.001; fructose 25%: 0.072 g/L 95%CI [-0.004 to 0.148], P = 0.074 versus aspartame). The post hoc analyses showed significant interactive effects of fructose*glucose on LDL-C and apoB (both P < 0.01), but not on 24-h triglyceride (P = 0.340). CONCLUSION A significant interaction between fructose and glucose contributed to increases of lipoprotein risk factors when the two monosaccharides were co-ingested as HFCS. Thus, the effects of HFCS on lipoprotein risks factors are not solely mediated by the fructose content and it cannot be assumed that glucose is a benign component of HFCS. Our findings suggest that HFCS may be as harmful as isocaloric amounts of pure fructose and provide further support for the urgency to implement strategies to limit free sugar consumption.