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New advances in renal mechanisms of high fructose-induced salt-sensitive hypertension.
Xu, CM, Yang, TX
Sheng li xue bao : [Acta physiologica Sinica]. 2018;(6):581-590
Abstract
Fructose intake has increased dramatically over the past century and the upward trend has continued until recently. Increasing evidence suggests that the excessive intake of fructose induces salt-sensitive hypertension. While the underlying mechanism is complex, the kidney likely plays a major role. This review will highlight recent advances in the renal mechanisms of fructose-induced salt-sensitive hypertension, including (pro)renin receptor-dependent activation of intrarenal renin-angiotensin system, increased nephron Na+ transport activity via sodium/hydrogen exchanger 3 and Na/K/2Cl cotransporter, increased renal uric acid production, decreased renal nitric oxide production, and increased renal reactive oxygen species production, and suggest actions based on these mechanisms that have therapeutic implications.
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The Influence of Pre-Exercise Glucose versus Fructose Ingestion on Subsequent Postprandial Lipemia.
Yang, TJ, Chiu, CH, Tseng, MH, Chang, CK, Wu, CL
Nutrients. 2018;(2)
Abstract
Ingestion of low glycemic index (LGI) carbohydrate (CHO) before exercise induced less insulin response and higher fat oxidation than that of high GI (HGI) CHO during subsequent exercise. However, the effect on the subsequent postprandial lipid profile is still unclear. Therefore, the aim of this study was to investigate ingestion of CHO drinks with different GI using fructose and glucose before endurance exercise on the subsequent postprandial lipid profile. Eight healthy active males completed two experimental trials in randomized double-blind cross-over design. All participants ingested 500 mL CHO (75 g) solution either fructose (F) or glucose (G) before running on the treadmill at 60% VO₂max for 1 h. Participants were asked to take an oral fat tolerance test (OFTT) immediately after the exercise. Blood samples were obtained for plasma and serum analysis. The F trial was significantly lower than the G trial in TG total area under the curve (AUC; 9.97 ± 3.64 vs. 10.91 ± 3.56 mmol × 6 h/L; p = 0.033) and incremental AUC (6.57 ± 2.46 vs. 7.14 ± 2.64 mmol/L × 6 h, p = 0.004). The current data suggested that a pre-exercise fructose drink showed a lower postprandial lipemia than a glucose drink after the subsequent high-fat meal.
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Effects of fructose consumption on postprandial TAG: an update on systematic reviews with meta-analysis.
Macedo, RCO, Vieira, AF, Moritz, CEJ, Reischak-Oliveira, A
The British journal of nutrition. 2018;(4):364-372
Abstract
The aim of this study was to re-examine the chronic effect (>7 d) of fructose consumption on postprandial TAG, in adolescents and adults. The research was carried out in March 2017 and used different electronic databases, such as Medline ® (Pubmed®), Embase® and Cochrane. The review considered clinical trials (parallel or crossed) that evaluated the effect of fructose consumption for a period longer than 7 d, in humans. Two investigators independently performed data extraction. The outcome was the absolute delta of TAG concentration in a 4-h postprandial period. The results were presented with delta mean difference between treatments with 95 % CI. The calculations were made based on random-effect models. Statistical heterogeneity of treatment effects between studies was assessed by Cochrane's 'Q Test' and 'I 2' inconsistency test. The meta-analysis of the twelve selected interventions (n 318) showed that fructose generated larger variation (δ) of TAG concentrations during the postprandial period, compared with other carbohydrates (mean difference: 8·02 (95 % CI 0·46, 15·58) mg/dl (0·09 (95 % CI 0·01, 0·18) mmol/l); I 2: 74 %). High heterogeneity was generated almost exclusively by one study, and its withdrawal did not alter the result. We concluded that chronic consumption of fructose (>7 d) has a negative role on postprandial TAG in healthy adolescents and adults, as well as in overweight/obese individuals, but not in diabetics.
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Postexercise Fructose-Maltodextrin Ingestion Enhances Subsequent Endurance Capacity.
Maunder, E, Podlogar, T, Wallis, GA
Medicine and science in sports and exercise. 2018;(5):1039-1045
Abstract
PURPOSE Restoring skeletal muscle and hepatic glycogen content during short-term (<6 h) recovery from prolonged exercise is pertinent for athletes seeking to maximize performance in repeated exercise bouts. Previous research suggests that coingestion of fructose-glucose carbohydrate sources augments hepatic and has equivalent effects on skeletal muscle glycogen storage during short-term recovery from prolonged exercise compared with isocaloric glucose ingestion. The aim of the present investigation was to determine whether this has a discernible effect on subsequent exercise capacity. METHODS Eight trained endurance runners and triathletes performed two experimental trials in a single-blind, randomized, and counterbalanced crossover design. Trials involved treadmill running to exhaustion at 70% V˙O2max, a 4-h recovery with 90 g·h of glucose-maltodextrin (GLU + MAL) or fructose-maltodextrin (FRU + MAL) ingestion (1:1.5 ratio), and a second bout of treadmill running to exhaustion at 70% V˙O2max. RESULTS Exercise capacity in bout 2 was significantly greater with FRU + MAL (81.4 ± 22.3 vs 61.4 ± 9.6 min, P = 0.02), a large magnitude effect (effect size = 1.84 ± 1.12, 32.4% ± 19.9%). Total carbohydrate oxidation rates were not significantly different during bout 1 or 2 between trials, although total carbohydrate oxidized in bout 2 was significantly greater with FRU + MAL (223 ± 66 vs 157 ± 26 g, P = 0.02). Ingested carbohydrate oxidation rates were greater during bout 2 with FRU + MAL (P = 0.001). Plasma glucose and nonesterified fatty acid concentrations were not significantly different between trials. Plasma lactate concentrations were significantly greater during recovery before bout 2 with FRU + MAL (P = 0.001). Self-reported nausea and stomach fullness during bout 2 were marginally in favor of FRU + MAL. CONCLUSION Short-term recovery of endurance capacity was significantly enhanced with FRU + MAL versus GLU + MAL ingestion during recovery.
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Dietary carbohydrates and fatty liver disease: de novo lipogenesis.
Chiu, S, Mulligan, K, Schwarz, JM
Current opinion in clinical nutrition and metabolic care. 2018;(4):277-282
Abstract
PURPOSE OF REVIEW To review recent evidence for the role of dietary carbohydrate in de novo lipogenesis (DNL) and nonalcoholic fatty liver disease (NAFLD). RECENT FINDINGS A large body of evidence suggests that increased hepatic DNL is a significant pathway contributing to the development of NAFLD. Dietary carbohydrates, in particular, fructose, have been shown to stimulate DNL and increase liver fat, although it is debated whether this is due to excess energy or fructose per se. Recent dietary intervention studies conducted in energy balance show that high-fructose diets increase DNL and liver fat, whereas fructose restriction decreases DNL and liver fat. SUMMARY The association of high-carbohydrate and high-sugar diets with NAFLD may in part be explained by the effect of sugar on increasing hepatic DNL.
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Acute metabolic and endocrine responses induced by glucose and fructose in healthy young subjects: A double-blinded, randomized, crossover trial.
Cai, W, Li, J, Shi, J, Yang, B, Tang, J, Truby, H, Li, D
Clinical nutrition (Edinburgh, Scotland). 2018;(2):459-470
Abstract
BACKGROUND AND OBJECTIVE A rise in fructose consumption has been implicated in the etiology of obesity, diabetes and cardiovascular disease. Serum uric acid (UA) elevates after fructose ingestion, increasing the risk of cardiovascular disease. However, the impact of fructose ingestion on nitric oxide (NO) has not yet been confirmed. The aim of this study was to investigate the postprandial metabolic and endocrine responses following an acute ingestion of fructose and glucose in healthy subjects. METHOD This was a double-blinded, randomized, crossover postprandial trial. Eighteen healthy young subjects (9 males and 9 females) with a mean age of 23.6 ± 2.3 years and mean BMI of 20.2 ± 1.5 kg/m2 completed the experiment that was conducted in Hangzhou, China. Volunteers were randomized to two groups (A and B): after an 8-h overnight fast, volunteers either ingested 300 mL of 25% glucose (group A) or fructose (group B) solution at 0830 within 5 min. After a one-week washout period, volunteers were crossed over to receive the alternate test solution. Blood pressure was measured at 0 h, 1 h, 2 h and 3 h and venous blood was drawn at 0 h, 0.5 h, 1 h, 2 h and 3 h after ingestion of the test solution. RESULTS Eighteen subjects completed the study. Serum NO level tended to be lower at 1 h (59.40 ± 3.10 μmol/L and 68.1 ± 3.40 μmol/L, respectively, p ≤ 0.05) and 2 h (62.70 ± 3.10 μmol/L and 70.10 ± 3.50 μmol/L, respectively, p ≤ 0.05) after fructose ingestion than after glucose. The 3-h AUC (area under curve) of NO was significantly lower after fructose ingestion than after glucose (p ≤ 0.05). UA level was higher at 1 h (512.17 ± 17.74 μmol/L and 372.11 ± 17.41 μmol/L, respectively, p ≤ 0.01) and 2 h (440.22 ± 16.07 μmol/L and 357.39 ± 14.80 μmol/L, respectively, p ≤ 0.05) after fructose ingestion than after glucose. The 3-h AUC of UA was significantly higher after fructose ingestion than after glucose (p ≤ 0.01). Correlation analyses revealed that NO was negatively associated with UA at T0.5h (r = -0.62, p ≤ 0.01), T1.0h (r = -0.69, p ≤ 0.001), T2.0h (r = -0.86, p ≤ 0.001) and T3.0h (r = -0.85, p ≤ 0.001) after fructose ingestion. SBP (systolic blood pressure) tended to be higher at 1 h (125.33 ± 1.95 mmHg and 112.06 ± 1.77 mmHg, respectively, p ≤ 0.05) after fructose ingestion than after glucose. The 3-h AUC of SBP was significantly higher after fructose ingestion than after glucose (p ≤ 0.05). The 3 h-AUC of TG, TC, HDL-C and LDL-C showed no differences between fructose and glucose. LDH (lactate dehydrogenase) level was higher at 1 h (195.00 ± 5.6 U/L and 177.67 ± 6.8 U/L, respectively, p ≤ 0.05) and 2 h (197.01 ± 6.32 U/L and 185.50 ± 7.37 U/L, respectively, p ≤ 0.05) after fructose ingestion than after glucose. The 3-h AUC of LDH was significantly higher after fructose ingestion than after glucose (p ≤ 0.05). AR was significantly higher at 1 h (19.86 ± 0.52 ng/mg Hb and 16.98 ± 0.29 ng/mg Hb, respectively, p ≤ 0.05) after fructose ingestion than after glucose. The 3-h AUC of AR (p ≤ 0.05) was significantly higher after fructose ingestion than after glucose (p ≤ 0.05). CONCLUSION Ingestion of a 75 g fructose load led to acute but unfavorable changes in certain metabolic and endocrine responses including increased serum concentrations and 3 h-AUC of UA, AR and LDH, increased SBP, and decreased endothelial NO production when compared with the same amount of ingested glucose.
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Fructose metabolism, cardiometabolic risk, and the epidemic of coronary artery disease.
Mirtschink, P, Jang, C, Arany, Z, Krek, W
European heart journal. 2018;(26):2497-2505
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Abstract
Despite strong indications that increased consumption of added sugars correlates with greater risks of developing cardiometabolic syndrome (CMS) and cardiovascular disease (CVD), independent of the caloric intake, the worldwide sugar consumption remains high. In considering the negative health impact of overconsumption of dietary sugars, increased attention is recently being given to the role of the fructose component of high-sugar foods in driving CMS. The primary organs capable of metabolizing fructose include liver, small intestine, and kidneys. In these organs, fructose metabolism is initiated by ketohexokinase (KHK) isoform C of the central fructose-metabolizing enzyme KHK. Emerging data suggest that this tissue restriction of fructose metabolism can be rescinded in oxygen-deprived environments. In this review, we highlight recent progress in understanding how fructose metabolism contributes to the development of major systemic pathologies that cooperatively promote CMS and CVD, reference recent insights into microenvironmental control of fructose metabolism under stress conditions and discuss how this understanding is shaping preventive actions and therapeutic approaches.
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Identification of Bacterial Species That Can Utilize Fructose-Asparagine.
Sabag-Daigle, A, Wu, J, Borton, MA, Sengupta, A, Gopalan, V, Wrighton, KC, Wysocki, VH, Ahmer, BMM
Applied and environmental microbiology. 2018;(5)
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Abstract
Salmonella enterica serovar Typhimurium is the only organism demonstrated to utilize fructose-asparagine (F-Asn) as a source of carbon and nitrogen. In this report, we first used a bioinformatics approach to identify other microorganisms that encode homologs of the Salmonella F-Asn utilization enzymes FraB (deglycase), FraD (kinase), and FraE (asparaginase). These candidate organisms were then tested with up to four different methods to confirm their ability to utilize F-Asn. The easiest and most broadly applicable method utilized a biological toxicity assay, which is based on the observation that F-Asn is toxic to a Salmonella fraB mutant. Candidate organisms were grown in a rich medium containing F-Asn, and depletion of F-Asn from the medium was inferred by the growth of a Salmonella fraB mutant in that same medium. For select organisms, the toxicity assay was cross-validated by direct mass spectrometry-aided measurement of F-Asn in the spent-culture media and through demonstration of FraB and FraD enzyme activity in cellular extracts. For prototrophs, F-Asn utilization was additionally confirmed by growth in a minimal medium containing F-Asn as the sole carbon source. Collectively, these studies established that Clostridiumbolteae, Clostridium acetobutylicum, and Clostridium clostridioforme can utilize F-Asn, but Clostridium difficile cannot; Klebsiella oxytoca and some Klebsiella pneumoniae subspecies can utilize F-Asn; and some Citrobacter rodentium and Citrobacter freundii strains can also utilize F-Asn. Within Salmonella enterica, the host-adapted serovars Typhi and Paratyphi A have lost the ability to utilize F-Asn.IMPORTANCE Fructose-asparagine (F-Asn) is a precursor to acrylamide that is found in human foods, and it is also a nutrient source for Salmonella enterica, a foodborne pathogen. Here, we determined that among the normal intestinal microbiota, there are species of Clostridium that encode the enzymes required for F-Asn utilization. Using complementary experimental approaches, we have confirmed that three members of Clostridium, two members of Klebsiella, and two members of Citrobacter can indeed utilize F-Asn. The Clostridium spp. likely compete with Salmonella for F-Asn in the gut and contribute to competitive exclusion. FraB, one of the enzymes in the F-Asn utilization pathway, is a potential drug target because inhibition of this enzyme leads to the accumulation of a toxic metabolite that inhibits the growth of Salmonella species. This study identifies the potential off-target organisms that need to be considered when developing therapeutics directed at FraB.
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Fructose, Glucocorticoids and Adipose Tissue: Implications for the Metabolic Syndrome.
Legeza, B, Marcolongo, P, Gamberucci, A, Varga, V, Bánhegyi, G, Benedetti, A, Odermatt, A
Nutrients. 2017;(5)
Abstract
The modern Western society lifestyle is characterized by a hyperenergetic, high sugar containing food intake. Sugar intake increased dramatically during the last few decades, due to the excessive consumption of high-sugar drinks and high-fructose corn syrup. Current evidence suggests that high fructose intake when combined with overeating and adiposity promotes adverse metabolic health effects including dyslipidemia, insulin resistance, type II diabetes, and inflammation. Similarly, elevated glucocorticoid levels, especially the enhanced generation of active glucocorticoids in the adipose tissue due to increased 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) activity, have been associated with metabolic diseases. Moreover, recent evidence suggests that fructose stimulates the 11β-HSD1-mediated glucocorticoid activation by enhancing the availability of its cofactor NADPH. In adipocytes, fructose was found to stimulate 11β-HSD1 expression and activity, thereby promoting the adipogenic effects of glucocorticoids. This article aims to highlight the interconnections between overwhelmed fructose metabolism, intracellular glucocorticoid activation in adipose tissue, and their metabolic effects on the progression of the metabolic syndrome.
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Fructose replacement of glucose or sucrose in food or beverages lowers postprandial glucose and insulin without raising triglycerides: a systematic review and meta-analysis.
Evans, RA, Frese, M, Romero, J, Cunningham, JH, Mills, KE
The American journal of clinical nutrition. 2017;(2):506-518
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Background: Conflicting evidence exists on the effects of fructose consumption in people with type 1 and type 2 diabetes mellitus. No systematic review has addressed the effect of isoenergetic fructose replacement of glucose or sucrose on peak postprandial glucose, insulin, and triglyceride concentrations.Objective: The objective of this study was to review the evidence for postprandial glycemic and insulinemic responses after isoenergetic replacement of either glucose or sucrose in foods or beverages with fructose.Design: We searched the Cochrane Library, MEDLINE, EMBASE, the WHO International Clinical Trials Registry Platform Search Portal, and clinicaltrials.gov The date of the last search was 26 April 2016. We included randomized controlled trials measuring peak postprandial glycemia after isoenergetic replacement of glucose, sucrose, or both with fructose in healthy adults or children with or without diabetes. The main outcomes analyzed were peak postprandial blood glucose, insulin, and triglyceride concentrations.Results: Replacement of either glucose or sucrose by fructose resulted in significantly lowered peak postprandial blood glucose, particularly in people with prediabetes and type 1 and type 2 diabetes. Similar results were obtained for insulin. Peak postprandial blood triglyceride concentrations did not significantly increase.Conclusions: Strong evidence exists that substituting fructose for glucose or sucrose in food or beverages lowers peak postprandial blood glucose and insulin concentrations. Isoenergetic replacement does not result in a substantial increase in blood triglyceride concentrations.