Form Of High-fructose Corn Syrup Research Articles

The Effect of Different Fructose Diets on the Lifespan of C. elegans

Sugar, such as fructose, is widely known to be a dietary cause for many health complications including diabetes, heart disease, and even cancer, and is an enticing yet harmful substance if consumed in large quantities. Fructose, typically in the form of high-fructose corn syrup, is the sugar most commonly found in fast foods. Thus, we chose to study the health effects of a high fructose diet on humans through experimentation on Caenorhabditis elegans, which are effective model organisms due to their rapid reproduction rate and stability despite variations in environmental conditions. We hypothesized that increasing sugar intake in C. elegans will reduce C. elegans survival, though moderate amounts of sugar may increase survival. The results show that the concentration of fructose had a significant influence on the survival rate of C. elegans. The C. elegans receiving 0% and 5% fructose concentration treatments had much higher survival rates than the 15% plates, which had zero surviving C. elegans after six days. After statistical analysis, the 5% and 15% plates were determined to yield significantly different survival rates. Thus, there is sufficient data to conclude that diets containing high levels of fructose negatively impact C. elegans life, suggesting that diets high in sugars such as high fructose corn syrup are harmful to humans. However, it was not possible to discern any significant difference between the 0% and 5% treatments from the data generated. Further experimentation would be needed to investigate the effects of diets containing a moderate amount of sugar.

Sugar intake and expectation effects on cognition and mood.

Glucose intake has been found to improve some aspects of cognitive performance; however, results are often inconsistent. This inconsistency may be related to expectations surrounding glucose, which can have strong effects on performance outcomes. The present study evaluated the independent and interactive effects of acute sugar intake, in the form of high-fructose corn syrup (HFCS), and sugar expectancies on cognitive performance and mood. One hundred five healthy young adults were randomized according to sugar intake and expectation: consumed-sugar/told-sugar, consumed-sugar/told-no-sugar, consumed-no-sugar/told-sugar, and consumed-no-sugar/told-no-sugar. Thirty minutes after sugar or no-sugar intake, participants completed the Profile of Mood States and a battery of cognitive tests, including immediate and delayed recall, the Stroop test, n-back task, and continuous performance task. Tension increased following the expectation of consuming sugar, regardless of sugar consumption (p < .05). On the continuous performance task, accuracy and sensitivity were higher (ps < .05) and false alarm rate was lower (p < .05) following sugar than no sugar intake. No effects of sugar intake or expectation were found for any other mood or cognitive measure (ps > .05). The findings suggest that sugar intake in the form of HFCS may benefit certain cognitive processes, such as those that require sustained attention, but that the expectation of sugar intake is not sufficient to produce such benefits. (PsycINFO Database Record

Fructose Contents of Various Popular Sweetened Beverages based on Milk Using by HPLC

The global consumption of fructose in the form of high-fructose corn syrup (HFCS) has increased considerably over the past several decades. The current intake of HFCS exceeds that of other major caloric sweeteners such as sucrose. Fructose has potentially adverse effects on human metabolism. Therefore, the objective of this study was to analyze the monosaccharide contents of 13 sweetened milk-based beverages by using high-performance liquid chromatography (HPLC). The total monosaccharide (fructose and glucose) contents of various sweetened milk-based beverages ranged from 0.60 g/100 mL (cheese) to 26.03 g/100 mL (maple caramel snack), while milk showed only 0 g/100 mL monosaccharides. The fructose-to-glucose ratio of various popular sweetened milk-based beverages ranged from not-detected (ND) to 2.24 g/100 mL, but the content of glucose was higher than that of fructose in only three samples, namely, strawberry flavored milk, shrimp chips, and maple caramel snack. The analyzed results revealed important basic information about monosaccharides in various milk-based sweetened beverages, presenting ideas for future fructose research.

The role of fructose in metabolism and cancer

Fructose consumption has dramatically increased in the last 30 years. The principal form has been in the form of high-fructose corn syrup found in soft drinks and processed food. The effect of excessive fructose consumption on human health is only beginning to be understood. Fructose has been confirmed to induce several obesity-related complications associated with the metabolic syndrome. Here we present an overview of fructose metabolism and how it contrasts with that of glucose. In addition, we examine how excessive fructose consumption can affect de novo lipogenesis, insulin resistance, inflammation, and reactive oxygen species production. Fructose can also induce a change in the gut permeability and promote the release of inflammatory factors to the liver, which has potential implications in increasing hepatic inflammation. Moreover, fructose has been associated with colon, pancreas, and liver cancers, and we shall discuss the evidence for these observations. Taken together, data suggest that sustained fructose consumption should be curtailed as it is detrimental to long-term human health.

The good, the bad, and the unknown: Fructose and FGF21.

In this issue of Molecular Metabolism, Dushay et al. report new results demonstrating fructose ingestion in humans acutely and robustly raises circulating levels of fibroblast growth factor 21 (FGF21) [1], a recently discovered hormone that has been proposed to have beneficial effects on metabolic health, including reduction of body weight and improvements of glucose and lipid metabolism [2]. People suffering from the metabolic syndrome have higher baseline circulating FGF21 levels and exhibit a larger increase of plasma FGF21 concentrations following an oral fructose load. In contrast, the increase of FGF21 after ingestion of the same amount of glucose was delayed and much more modest. These results are paradoxical in that the metabolic effects of FGF-21 appear to be mainly beneficial while those of dietary fructose are generally deleterious [3]. The authors suggest the possibility that obese subjects with metabolic syndrome are resistant to the actions of FGF21 (akin to augmentation of circulating insulin and leptin concentrations and responses in insulin and leptin resistance) and that the exaggerated response to fructose ingestion may be a compensatory response [1]. The increases of FGF-21 in response to fructose ingestion across normal weight and overweight/obese subjects was significantly correlated with circulating insulin and glucose levels in response to oral glucose loads suggesting a relationship between FGF21 and insulin senstivity/glucose tolerance. Together, these novel results shed light on a potential mechanism related to the adverse metabolic effects of dietary fructose and raise new questions about the nutritional regulation of metabolic responses to dietary macronutrients, specifically sugars.

Fructose and Glucose Ingestion Affect Appetite Pathways in the Brain Differently

Fructose (usually in the form of high-fructose corn syrup) is added to processed foods and beverages because it is more intensely sweet than glucose —

Sugar Making Sugar: Gluconeogenesis Triggered by Fructose via a Hypothalamic-Adrenal-Corticosterone Circuit

Sugar Making Sugar: Gluconeogenesis Triggered by Fructose via a Hypothalamic-Adrenal-Corticosterone Circuit

Fructose Malabsorption and Intolerance: Effects of Fructose with and without Simultaneous Glucose Ingestion

Concern exists that increasing fructose consumption, particularly in the form of high-fructose corn syrup, is resulting in increasing rates of fructose intolerance and aggravation of clinical symptoms in individuals with irritable bowel syndrome. Most clinical trials designed to test this hypothesis have used pure fructose, a form not commonly found in the food supply, often in quantities and concentrations that exceed typical fructose intake levels. In addition, the amount of fructose provided in tests for malabsorption, which is thought to be a key cause of intolerance, often exceeds the normal physiological absorption capacity for this sugar. To help health professionals accurately identify and treat this condition, this article reviews clinical data related to understanding fructose malabsorption and intolerance (i.e., malabsorption that manifests with symptoms) relative to usual fructose and other carbohydrate intake. Because simultaneous consumption of glucose attenuates fructose malabsorption, information on the fructose and glucose content of foods, beverages, and ingredients representing a variety of food categories is provided.

Impact of Fructose Consumption on Gene Expression: Role of miRNAs

The metabolic syndrome (MS), a group of symptoms including elevated blood pressure and plasma fasting glucose, dyslipidemia, and obesity, has been on the rise, reaching a prevalence of 36% in the US. In proportion is an increase of fructose in soft drinks in the form of high-fructose corn syrup. MS significantly increases the risk of cardiovascular disease, and we have previously shown that FC disrupts the regulation of O2 consumption in the heart by lowering NO bioavailability through the generation of superoxide. Presently, we explored the molecular effects of FC. SD rats were fed a normal or a 60% fructose diet for 21 days. mRNA microarray analysis of cardiac tissue revealed significant changes in 238 genes (p<0.05, fold change at least ±1.5), including upregulation of the nuclear receptor Pparα, cholesterol transporter caveolin 1, and endothelin receptor B, and downregulation of Mrpl1 2, a mitochondrial ribosomal protein, and Atp5S, which encodes a subunit of mitochondrial ATP synthase. miRNA microarray analysis showed corresponding downregulation of miRNAs associated with upregulated genes and vice versa, including upregulation of miR126, a regulator of angiogenesis, and miR21, which is significantly upregulated in heart failure (downregulation of protein). Conclusion FC triggers gene expression changes in the heart with involvement of miRNAs, suggesting an underlying mechanism behind the effects of FC.

The Role of Salt in the Pathogenesis of Fructose-Induced Hypertension

Metabolic syndrome, as manifested by visceral obesity, hypertension, insulin resistance, and dyslipidemia, is reaching epidemic proportions in the Western World, specifically the United States. Epidemiologic studies suggest that the increased prevalence of metabolic syndrome directly correlates with an increase in the consumption of fructose, mainly in the form of high-fructose corn syrup. This inexpensive alternative to traditional sugar has been increasingly utilized by the food industry as a sweetener since the 1960s. While augmented caloric intake and sedentary lifestyles play important roles in the increasing prevalence of obesity, the pathogenesis of hypertension in metabolic syndrome remains controversial. One intriguing observation points to the role of salt in fructose-induced hypertension. Recent studies in rodents demonstrate that increased dietary fructose intake stimulates salt absorption in the small intestine and kidney tubules, resulting in a state of salt overload, thus setting in motion a cascade of events that will lead to hypertension. These studies point to a novel interaction between the fructose-absorbing transporter, Glut5, and the salt transporters, NHE3 and PAT1, in the intestine and kidney proximal tubule. This paper will focus on synergistic roles of fructose and salt in the pathogenesis of hypertension resulting from salt overload.

Dietary fructose, salt absorption and hypertension in metabolic syndrome: towards a new paradigm.

The worldwide increase in the incidence of metabolic syndrome correlates with marked increase in total fructose intake in the form of high-fructose corn syrup, beverage and table sugar. Increased dietary fructose intake in rodents has been shown to recapitulate many aspects of metabolic syndrome by causing hypertension, insulin resistance and hyperlipidaemia. Recent studies demonstrated that increased dietary fructose intake stimulates salt absorption in the small intestine and kidney tubules, resulting in a state of salt overload and thus causing hypertension. The absorption of salt (sodium and chloride) in the small intestine is predominantly mediated via the chloride/base exchangers DRA (Down Regulated in Adenoma) (SLC26A3) and PAT1 (Putative Anion Transporter 1) (SLC26A6), and the Na(+) /H(+) exchanger NHE3 (Sodium Hydrogen Exchanger3) (SLC9A3). PAT1 and NHE3 also co-localize on the apical membrane of kidney proximal tubule. Luminal fructose stimulated salt absorption in the jejunum and kidney tubules, responses that were significantly diminished in PAT1 null mice. These studies further demonstrated that Glut5 (SLC2A5) is the major fructose-absorbing transporter in the small intestine (and kidney proximal tubule) and plays an essential role in the systemic homeostasis of fructose. Increased dietary fructose intake for several weeks upregulated the expression of NHE3, PAT1 and Glut5 in the intestine and resulted in hypertension in wild-type mice, a response that was almost abolished in PAT1 null mice and abrogated in Glut5 null mice. This article will discuss the interaction of Glut5 with salt-absorbing transporters and review the role of dietary fructose in enhanced salt absorption in intestine and kidney as it relates to the pathogenesis of hypertension in metabolic syndrome.

Effects of high-fructose corn syrup and sucrose consumption on circulating glucose, insulin, leptin, and ghrelin and on appetite in normal-weight women

Objective Fructose has been implicated in obesity, partly due to lack of insulin-mediated leptin stimulation and ghrelin suppression. Most work has examined effects of pure fructose, rather than high-fructose corn syrup (HFCS), the most commonly consumed form of fructose. This study examined effects of beverages sweetened with HFCS or sucrose (Suc), when consumed with mixed meals, on blood glucose, insulin, leptin, ghrelin, and appetite. Methods Thirty lean women were studied on two randomized 2-d visits during which HFCS- and Suc-sweetened beverages were consumed as 30% of energy on isocaloric diets during day 1 while blood was sampled. On day 2, food was eaten ad libitum. Subjects rated appetite at designated times throughout visits. Results No significant differences between the two sweeteners were seen in fasting plasma glucose, insulin, leptin, and ghrelin ( P > 0.05). The within-day variation in all four items was not different between the two visits ( P > 0.05). Net areas under the curve were similar for glucose, insulin, and leptin ( P > 0.05). There were no differences in energy or macronutrient intake on day 2. The only appetite variable that differed between sweeteners was desire to eat, which had a higher area under the curve the day after Suc compared with HFCS. Conclusion These short-term results suggest that, when fructose is consumed in the form of HFCS, the measured metabolic responses do not differ from Suc in lean women. Further research is required to examine appetite responses and to determine if these findings hold true for obese individuals, males, or longer periods.

Beverage consumption and risk of obesity among Native Americans in Arizona.

Native Americans face some of the highest rates of obesity and diabetes in the world. Despite numerous education programs to reduce obesity among Native Americans, little attention has been paid to reducing fructose, particularly in the form of high-fructose corn syrup in beverages. Considerable data indicate that energy from beverages does not displace energy from other foods throughout the day, often leading to energy imbalance, and numerous studies have documented that beverages are a leading contributor to energy intakes among Native Americans. Prevention programs that target pregnant women and parents of infants and very young children are necessary to halt the epidemic of obesity among Native Americans; one approach may be by promoting sugar-free beverages.