Explore the vast range of titles available.

Excessive consumption of beverages sweetened with high-fructose corn syrup (HFCS) is associated with obesity and with an increased risk of colorectal cancer. Whether HFCS contributes directly to tumorigenesis is unclear. We investigated the effects of daily oral administration of HFCS in adenomatous polyposis coli (APC) mutant mice, which are predisposed to develop intestinal tumors. The HFCS-treated mice showed a substantial increase in tumor size and tumor grade in the absence of obesity and metabolic syndrome. HFCS increased the concentrations of fructose and glucose in the intestinal lumen and serum, respectively, and the tumors transported both sugars. Within the tumors, fructose was converted to fructose-1-phosphate, leading to activation of glycolysis and increased synthesis of fatty acids that support tumor growth. These mouse studies support the hypothesis that the combination of dietary glucose and fructose, even at a moderate dose, can enhance tumorigenesis.

Fructose consumption is linked to the rising incidence of obesity and cancer, which are two of the leading causes of morbidity and mortality globally 1 , 2 . Dietary fructose metabolism begins at the epithelium of the small intestine, where fructose is transported by glucose transporter type 5 (GLUT5; encoded by SLC2A5 ) and phosphorylated by ketohexokinase to form fructose 1-phosphate, which accumulates to high levels in the cell 3 , 4 . Although this pathway has been implicated in obesity and tumour promotion, the exact mechanism that drives these pathologies in the intestine remains unclear. Here we show that dietary fructose improves the survival of intestinal cells and increases intestinal villus length in several mouse models. The increase in villus length expands the surface area of the gut and increases nutrient absorption and adiposity in mice that are fed a high-fat diet. In hypoxic intestinal cells, fructose 1-phosphate inhibits the M2 isoform of pyruvate kinase to promote cell survival 5 – 7 . Genetic ablation of ketohexokinase or stimulation of pyruvate kinase prevents villus elongation and abolishes the nutrient absorption and tumour growth that are induced by feeding mice with high-fructose corn syrup. The ability of fructose to promote cell survival through an allosteric metabolite thus provides additional insights into the excess adiposity generated by a Western diet, and a compelling explanation for the promotion of tumour growth by high-fructose corn syrup. A high-fructose diet in mice improves the survival of intestinal epithelial cells, which leads to an increase in gut surface area, enhanced absorption of lipids and the promotion of tumour growth and obesity.

The present commentary contains a clear and simple guide designed to identify ultra-processed foods. It responds to the growing interest in ultra-processed foods among policy makers, academic researchers, health professionals, journalists and consumers concerned to devise policies, investigate dietary patterns, advise people, prepare media coverage, and when buying food and checking labels in shops or at home. Ultra-processed foods are defined within the NOVA classification system, which groups foods according to the extent and purpose of industrial processing. Processes enabling the manufacture of ultra-processed foods include the fractioning of whole foods into substances, chemical modifications of these substances, assembly of unmodified and modified food substances, frequent use of cosmetic additives and sophisticated packaging. Processes and ingredients used to manufacture ultra-processed foods are designed to create highly profitable (low-cost ingredients, long shelf-life, emphatic branding), convenient (ready-to-consume), hyper-palatable products liable to displace all other NOVA food groups, notably unprocessed or minimally processed foods. A practical way to identify an ultra-processed product is to check to see if its list of ingredients contains at least one item characteristic of the NOVA ultra-processed food group, which is to say, either food substances never or rarely used in kitchens (such as high-fructose corn syrup, hydrogenated or interesterified oils, and hydrolysed proteins), or classes of additives designed to make the final product palatable or more appealing (such as flavours, flavour enhancers, colours, emulsifiers, emulsifying salts, sweeteners, thickeners, and anti-foaming, bulking, carbonating, foaming, gelling and glazing agents).

This review aims to provide a historical reference of branched-chain amino acid (BCAA) metabolism and provide a link between peripheral and central nervous system (CNS) metabolism of BCAAs. Leucine, isoleucine, and valine (Leu, Ile, and Val) are unlike most other essential amino acids (AA), being transaminated initially in extrahepatic tissues, and requiring interorgan or intertissue shuttling for complete catabolism. Within the periphery, BCAAs are essential AAs and are required for protein synthesis, and are key nitrogen donors in the form of Glu, Gln, and Ala. Leucine is an activator of the mammalian (or mechanistic) target of rapamycin, the master regulator of cell growth and proliferation. The tissue distribution and activity of the catabolic enzymes in the peripheral tissues as well as neurological effects in Maple Syrup Urine Disease (MSUD) show the BCAAs have a role in the CNS. Interestingly, there are significant differences between murine and human CNS enzyme distribution and activities. In the CNS, BCAAs have roles in neurotransmitter synthesis, protein synthesis, food intake regulation, and are implicated in diseases. MSUD is the most prolific disease associated with BCAA metabolism, affecting the branched-chain α-keto acid dehydrogenase complex (BCKDC). Mutations in the branched-chain aminotransferases (BCATs) and the kinase for BCKDC also result in neurological dysfunction. However, there are many questions of BCAA metabolism in the CNS (as well as the periphery) that remain elusive. We discuss areas of BCAA and BCKA metabolism that have yet to be researched adequately.

We tested the hypothesis that ingestion of a caffeinated soft drink sweetened with high‐fructose corn syrup acutely increases arterial stiffness. In a randomized counterbalanced, crossover design, fourteen healthy adults (25 ± 3 years, 6 women) reported to the laboratory for two experimental visits where 500 ml of tap water (H2O) or 500 ml of Mountain Dew® (a caffeinated soft drink sweetened with high‐fructose corn syrup (HFCS)) were consumed. Arterial stiffness (carotid‐to‐femoral pulse wave velocity (cfPWV)), peripheral and central blood pressures were measured pre‐consumption, 30 min post‐consumption, and 120 min post‐consumption. Prior to each measurement period, beat‐to‐beat hemodynamic measures were collected. Changes in heart rate, blood pressure, and cardiac output from pre‐consumption did not differ between trials at any timepoint (p ≥ 0.06). Moreover, changes in peripheral or central blood pressures from pre‐consumption did not differ between trials (p ≥ 0.84). Likewise, changes in cfPWV from pre‐consumption to 30 min post‐consumption (HFCS: 0.2 ± 0.3 m/s, H2O: 0.0 ± 0.3 m/s, p = 0.34) and 120 min post‐consumption (HFCS: 0.3 ± 0.4 m/s, H2O: 0.2 ± 0.3 m/s, p = 0.77) did not differ. Changes in aortic augmentation pressure, augmentation index, augmentation index corrected to a heart rate of 75 bpm, and reflection magnitude did not differ between conditions at 30 min post‐ (p ≥ 0.55) or 120 min post‐ (p ≥ 0.18) consumption. In healthy young adults, ingesting 500 ml of a commercially available caffeinated soft drink sweetened with high‐fructose corn syrup does not acutely change indices of arterial stiffness and wave reflection. This study investigated whether the ingestion of a caffeinated soft drink sweetened with high‐fructose corn syrup acutely modified arterial stiffness. In a randomized counterbalanced, crossover design, fourteen young healthy adults consumed 500 ml of tap water or a caffeinated soft drink sweetened with high‐fructose corn syrup, after which carotid‐to‐femoral pulse wave velocity was measured. This study found that ingesting 500 ml of a commercially available caffeinated soft drink sweetened with high‐fructose corn syrup does not acutely change indices of arterial stiffness.

This study aimed to experimentally investigate the effect of sugar syrup additions on quality measurements of honey and to detect adulteration. For that purpose, two different pure blossom honey samples were adulterated by directly mixing 0%, 5%, 10%, 20%, 30%, 40%, and 50% of commercially available glucose–fructose corn syrup and maltose corn syrup. In this regard, key physico-chemical properties like moisture, pH, free acidity, proline, diastase number, color (L, a, b and Delta-E), electrical conductivity, HMF, sugar profile (glucose, fructose, sucrose and maltose), and C4 sugar analysis were tested. The results of the individual analysis of moisture, pH, free acidity, proline, diastase number, color, electrical conductivity, and HMF failed to detect sugar syrup adulteration. However, when principal component analysis (PCA) was utilized to analyze the data gathered from these tests, adulterations at all-syrup ratios (5–50%) were successfully detected.

Labels do not disclose the excess-free-fructose/unpaired-fructose content in foods/beverages. Objective was to estimate excess-free-fructose intake using USDA loss-adjusted-food-availability (LAFA) data (1970–2019) for high fructose corn syrup (HFCS) and apple juice, major sources of excess-free-fructose, for comparison with malabsorption dosages (~ 5 g-children/ ~ 10 g-adults). Unlike sucrose and equimolar fructose/glucose, unpaired-fructose triggers fructose malabsorption and its health consequences. Daily intakes were calculated for HFCS that is generally-recognized-as-safe/ (55% fructose/45% glucose), and variants (65/35, 60/40) with higher fructose-to-glucose ratios (1.9:1, 1.5:1), as measured by independent laboratories. Estimations include consumer-level-loss (CLL) allowances used before (20%), and after, subjective, retroactively-applied increases (34%), as recommended by corn-refiners (~ 2012). No contributions from crystalline-fructose or agave syrup were included due to lack of LAFA data. High-excess-free-fructose-fruits (apples/pears/watermelons/mangoes) were not included. Eaten in moderation they are less likely to trigger malabsorption. Another objective was to identify potential parallel trends between excess-free-fructose intake and the “unexplained” US asthma epidemic. The fructose/gut-dysbiosis/lung axis is well documented, case-study evidence and epidemiological research link HFCS/apple juice intake with asthma, and unlike gut-dysbiosis/gut-fructosylation, childhood asthma prevalence data spans > 40 years. Results Excess-free-fructose daily intake for individuals consuming HFCS with an average 1.5:1 fructose-to-glucose ratio, ranged from 0.10 g/d in 1970, to 11.3 g/d in 1999, to 6.5 g/d in 2019, and for those consuming HFCS with an average 1.9:1 ratio, intakes ranged from 0.13 g/d to 16.9 g/d (1999), to 9.7 g/d in 2019 , based upon estimates with a 20% CLL allowance. Intake exceeded dosages that trigger malabsorption (~ 5 g) around ~ 1980. By the early 1980’s, tripled apple juice intake had added ~ 0.5 g to average-per-capita excess-free-fructose intake. Contributions were higher (~ 3.8 g /4-oz.) for individuals consuming apple juice consistent with a healthy eating pattern (4-oz. children, 8-oz. adults). The “unexplained” childhood asthma epidemic (1980-present) parallels increasing average-per-capita HFCS/apple juice intake trends and reflects epidemiological research findings. Conclusion Displacement of sucrose with HFCS, its ubiquitous presence in the US food-supply, the industry practice of adding more fructose to HFCS than generally-recognized-as-safe, and increased use of apple juice/crystalline fructose/agave syrup in foods/beverages has contributed to unprecedented excess-free-fructose intake levels, fructose malabsorption, gut-dysbiosis and gut-fructosylation (immunogen burden)-gateways to chronic disease.

Fructose consumption has increased considerably over the past five decades, largely due to the widespread use of high-fructose corn syrup as a sweetener 1 . It has been proposed that fructose promotes the growth of some tumours directly by serving as a fuel 2 , 3 . Here we show that fructose supplementation enhances tumour growth in animal models of melanoma, breast cancer and cervical cancer without causing weight gain or insulin resistance. The cancer cells themselves were unable to use fructose readily as a nutrient because they did not express ketohexokinase-C (KHK-C). Primary hepatocytes did express KHK-C, resulting in fructolysis and the excretion of a variety of lipid species, including lysophosphatidylcholines (LPCs). In co-culture experiments, hepatocyte-derived LPCs were consumed by cancer cells and used to generate phosphatidylcholines, the major phospholipid of cell membranes. In vivo, supplementation with high-fructose corn syrup increased several LPC species by more than sevenfold in the serum. Administration of LPCs to mice was sufficient to increase tumour growth. Pharmacological inhibition of ketohexokinase had no direct effect on cancer cells, but it decreased circulating LPC levels and prevented fructose-mediated tumour growth in vivo. These findings reveal that fructose supplementation increases circulating nutrients such as LPCs, which can enhance tumour growth through a cell non-autonomous mechanism. Dietary fructose enhances tumour growth in animal models of melanoma, breast cancer and cervical cancer indirectly via metabolite transfer.

Short-chain fructooligosaccharides (sc-FOS) are prebiotics beneficial to human health, which can be synthesized from raw material containing a high sucrose content. Sugarcane syrup (SS) without molasses removal contains sucrose as a major sugar and is a rich source of several bioactive compounds. The aim of this study is to investigate factors affecting sc-FOS synthesis from SS using commercial enzyme preparations containing fructosyltransferase activity as biocatalysts. sc-FOS content increased significantly as the sucrose concentration of SS in the reaction mixture increased up to 40% (w/v). Changes in carbohydrate compositions during the transfructosylating reaction of a pure sucrose solution and SS prepared from the two sugarcane cultivars Khon Kaen 3 and Suphanburi 50, catalyzed by Pectinex Ultra SP-L and Viscozyme L, showed similar profiles. Both enzymes showed a high ability to transfer fructosyl moieties to produce sc-FOS and a plateau of the total sc-FOS concentration was observed after 4 h of reaction time. For the pure sucrose solution and SS (Suphanburi 50), Viscozyme showed a superior ability to convert sucrose to Pectinex, with a higher sc-FOS yield (g FOS/100 g of initial sucrose), GF2 or 1-kestose yield (g GF2/g of initial sucrose) and GF3 or nystose yield (g GF3/g of initial sucrose). sc-FOS syrup (FOS SS) and the foam-mat-dried syrup powder prepared from SS and FOS SS, respectively, contained a high total phenolic content and possessed higher antioxidant activities than those prepared from pure sucrose, but contained lower calories.

Glucose–fructose syrups were studied for the first time as a carbon source for the biosynthesis of citric acid (CA) by the yeast Yarrowia lipolytica . The producer Y. lipolytica VKM Y-2373 was selected, and the growth conditions were optimized (syrup concentration, 30 g/L; pH, 6.0; aeration, 20% of saturation). The study found that the concentration of ammonium sulfate in the medium had a significant impact on CA production by Y. lipolytica . The maximum CA production was observed at a concentration of 2 g/L (NH 4 ) 2 SO 4 , while concentrations of 1.5 and 3.0 g/L resulted in a decrease of 12 and 30%, respectively. Under the selected conditions, Y. lipolytica VKM Y-2373 produced 36.7 g/L CA in a medium containing glucose–fructose syrup with 52% glucose and 57.7 g/L CA with syrup containing 92% glucose.