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Cover Image: Use Fig.1A from CEP 12227. Placebo versus no drug in POTS, Maternal fructose modulates AMPK signalling, GABA(A) receptors role in the amygdala, 5-HT4 receptor and neural differentiation [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Very High Fructose Intake Increases Serum LDL-Cholesterol and Total Cholesterol: A Meta-Analysis of Controlled Feeding Trials" by Y. H. Zhang et al. in a 2013 issue.

The author reflects on the health effects of fructose. He argues that if high dose of fructose was toxic, then people consuming large amounts of fruits might experience adverse effects. According to him, the absence of harm from fruit consumption links to the slow digestion rate of fruit compared with a sugar-sweetened beverage that produces fructose concentrations. He opines that fructose in its natural form is not linked with adverse effects up to the limits of consumption.

A letter to the editor is presented in response to the article "Gut microbial adaptation to dietary consumption of fructose artificial sweeteners and sugar alcohols: implications for host-microbe interactions contributing to obesity," by A. N. Payne, C. Chassard, and C. Lacroix in the 2012 issue.

A response from the author of the article regarding the effects of fructose on obesity and gut microbiota in the previous issue is presented.

The article discusses papers in the January 2012 issue of "Experimental Diabetes Research," including a paper on the influence of autonomic dysfunction associated with aging and type 2 diabetes, a paper on the effects of high-fructose diet in producing cardiovascular and metabolic pathologies, and the impact of MMP9 on the healing of diabetic foot ulcers.

The article discusses the role that fructose consumption plays in cardiometabolic disease risk. It comments on a study examining the effects fructose consumption had on body composition and found a significant increase in the accumulation of visceral adipose tissue. It states fructose consumption led to dyslipidemia but glucose consumption didn't appear to influence lipids. It reports on a study of weight gain in children which concluded weight gain was more closely related to excess calories.

The article offers information related to nutrition and environmental medicine. It states that a 51-year old woman was presented with a liver failure using Black Cohosh in 2006. It mentions that Professor of Clinical Pediatrics doctor Lustig at the University of California associates the increase in obesity rate in the dependability in fructose. It also presents the use of synthetic chemicals to treat breast cancer.

Background: Consumption of fructose-rich diets in the United States is on the rise and thought to be associated with obesity and cardiometabolic diseases.Objective: We sought to determine the effects of antenatal exposure to high-fructose diet on offspring's development of metabolic syndrome-like phenotype and other cardiovascular disease risk factors later in life.Study Design: Pregnant C57BL/6J dams were randomly allocated to fructose solution (10% wt/vol, n = 10) or water (n = 10) as the only drinking fluid from day 1 of pregnancy until delivery. After weaning, pups were started on regular chow, and evaluated at 1 year of life. We measured percent visceral adipose tissue and liver fat infiltrates using computed tomography, and blood pressure using CODA nonivasive monitor. Intraperitoneal glucose tolerance testing with corresponding insulin concentrations were obtained. Serum concentrations of glucose, insulin, triglycerides, total cholesterol, leptin, and adiponectin were measured in duplicate using standardized assays. Fasting homeostatic model assessment was also calculated to assess insulin resistance. P values <.05 were considered statistically significant.Results: Maternal weight, pup number, and average weight at birth were similar between the 2 groups. Male and female fructose group offspring had higher peak glucose and area under the intraperitoneal glucose tolerance testing curve compared with control, and higher mean arterial pressure compared to control. Female fructose group offspring were heavier and had higher percent visceral adipose tissue, liver fat infiltrates, homeostatic model assessment of insulin resistance scores, insulin area under the intraperitoneal glucose tolerance testing curve, and serum concentrations of leptin, and lower concentrations of adiponectin compared to female control offspring. No significant differences in these parameters were noted in male offspring. Serum concentrations of triglycerides or total cholesterol were not different between the 2 groups for either gender.Conclusion: Maternal intake of high fructose leads to fetal programming of adult obesity, hypertension, and metabolic dysfunction, all risk factors for cardiovascular disease. This fetal programming is more pronounced in female offspring. Limiting intake of high fructose-enriched diets in pregnancy may have significant impact on long-term health. [ABSTRACT FROM AUTHOR]

The authors reflect on a meta-analysis of clinical trials published within the issue, which evaluates the effects of fructose intake for persons with or without diabetes. They emphasize the difficulty in interpreting the meta-analysis and point out its conclusion on the added benefit of fructose in lowering concentrations of glycated hemoglobin. The need for controlled dose-response studies in different populations to measure the recommended amount of fructose consumption is suggested.

The article reports on the study conducted by Elizabeth Parks and colleagues at the University of Texas (UT) Southwestern Medical Center on trading the significance of fructose in losing weight in Texas. Researchers found that people who have low-carbohydrate diets lose weight because of their reduction in fructose intake. According to Elizabeth Parks, associate professor of clinical nutrition and lead author of a study, their study suggest that the right type of carbohydrates a person eats is just as important as the number of calories a person eats. They found that by limiting processed carbohydrates, many of which contain high-fructose corn syrup, help prevent weight gain.

Singh et al. offer exciting data in their new report about fructose-induced hypertension. Fructose induced an increase in serum uric acid after 8–10 weeks of increased fructose exposure, but no correlation was found between hyperuricemia and hypertension.Kidney International (2008) 74, 409–410. doi:10.1038/ki.2008.223 [ABSTRACT FROM AUTHOR]

The author reflects on research on the role of sugary drinks and fruit in increased risk of gout. He suggests that the research, which concluded that unsweetened fruit juices and fruit increased the incidence of gout and that sweetened soft drinks increase serum urate, support the idea that free fructose intake has an adverse effect on urate metabolism. He argues that the liberalization of the sugar trade may remove the demand for high fructose corn syrup and improve the health of consumers.

Taylor and Curhan report that consumption of fructose is independently associated with an increased risk of incident kidney stones. What could be the mechanisms underlying the relation between fructose intake and stone risk? And how should we incorporate this finding into the dietary advice that we give to our patients to prevent kidney stone formation?Kidney International (2008) 73, 139–140; doi:10.1038/sj.ki.5002700 [ABSTRACT FROM AUTHOR]

Explores the link between fructose and hypertension among Americans. Increase of fructose intake by Americans; Role of fructose in the prevalence of human obesity and metabolic syndrome, conditions that are closely associated with high blood pressure; Factors which contributed to the epidemic of human obesity in the U.S.

Metabolic syndrome can induce chronic kidney disease in humans. Genetically engineered mice on a C57BL/6 background are highly used for mechanistic studies. Although it has been shown that metabolic syndrome induces cardiovascular lesions in C57BL/6 mice, in depth renal phenotyping has never been performed. Therefore in this study we characterized renal function and injury in C57BL/6 mice with long-term metabolic syndrome induced by a high fat and fructose diet (HFFD). C57BL/6 mice received an 8 months HFFD diet enriched with fat (45% energy from fat) and drinking water enriched with fructose (30%). Body weight, food/water consumption, energy intake, fat/lean mass ratio, plasma glucose, HDL, LDL, triglycerides and cholesterol levels were monitored. At 3, 6 and 8 months, renal function was determined by inulin clearance and measure of albuminuria. At sacrifice, kidneys and liver were collected. Metabolic syndrome in C57BL/6 mice fed a HFFD was observed as early 4 weeks with development of type 2 diabetes at 8 weeks after initiation of diet. However, detailed analysis of kidney structure and function showed only minimal renal injury after 8 months of HFFD. HFFD induced moderate glomerular hyperfiltration (436,4 µL/min vs 289,8 µL/min; p-value=0.0418) together with a 2-fold increase in albuminuria only after 8 months of HFFD. This was accompanied by a 2-fold increase in renal inflammation (p-value=0.0217) but without renal fibrosis or mesangial matrix expansion. In addition, electron microscopy did not show alterations in glomeruli such as basal membrane thickening and foot process effacement. Finally, comparison of the urinary peptidome of these mice with the urinary peptidome from humans with diabetic nephropathy also suggested absence of diabetic nephropathy in this model. This study provides evidence that the HFFD C57BL/6 model is not the optimal model to study the effects of metabolic syndrome on the development of diabetic kidney disease. [ABSTRACT FROM AUTHOR]

The article presents several research highlights related to nephrology. It states the report by Turin and colleagues which discusses the association between longitudinal changes in estimated glomerular filtration rate (eGFR) and outpatient mortality. It notes the study on Bisphenol A (BPA)-associated adverse effects in children with low-grade albuminuria. It adds the study on the potential role of sodium restriction in preventing fructose kidney injury.

Introduction: L’utilisation de modèles animaux représente un outil indispensable dans la compréhension du diabète. Notre objectif est de mettre en place un modèle plus proche de la physiopathologie humaine, par une alimentation grasse et sucrée, et d’évaluer les conséquences métaboliques, oxydatives, systémiques et tissulaires. Matériels et méthodes: Les rats mâles Wistar recevant une alimentation standard ou grasse + 25 % fructose dans l’eau (HFHF) sont sacrifiés après 0, 2, 4, 8 mois (M) de régime. Nous évaluons le délai d’apparition du diabète (xM) et ses répercussions métaboliques (poids, glycémies, leptinémie), oxydatives (capacité antioxydante totale CAOT, péroxydation lipidique, carbonylation protéique), tissulaires (foie, pancréas, muscles, vaisseaux). Résultats: Le régime HFHF induit une augmentation du poids (1M), de la leptine (1M), un hyperinsulinisme (2M), une intolérance au glucose (2M), des hyperglycémies à jeun (6M). Les îlots pancréatiques présentent une hypertrophie (4M) associée à une augmentation de l’insuline (immunomarquage). Après 8M, une perte des gros/moyens îlots est associée à une diminution du contenu insulinique. Une stéatose hépatique (2M) s’accompagne d’une fibrose (8M). La production du glycogène hépatique est augmentée (4M). Un stress oxydant plasmatique est observé (augmentation des protéines carbonylées et de la CAOT (2M), des lipides péroxydés (4M)). Un stress oxydant tissulaire est visible dans l’ensemble des organes étudiés (2M). Conclusion: 6 mois de régime hyperlipidique/glucidique sont nécessaires pour développer un diabète de type 2, avec des répercussions tissulaires généralisées. Ce modèle permettra une meilleure compréhension de la physiopathologie du diabète et son évolution, dans le but unique de développer de nouvelles thérapies antidiabétiques préventives/curatives. [ABSTRACT FROM AUTHOR]

The article focuses on the relation of fructose to blood pressure, and the risk of obesity caused by fructose intake by individuals. It discusses uric acid as the intercessor of ill effects of fructose metabolism linking to metabolic byproduct that is being collected inside the body's organism. It also examines fructose metabolism which is directly damaging the cell due to decreasing levels of energy-shuttling molecule.

The article informs of a study which investigated the role played by high fructose diet in high blood pressure or hypertension.

The article discusses the increased risk of gout associated with fructose-containing soft drinks based on a study by Hyon K. Choi, presented at the Annual Meeting of the British Society for Rheumatology (BSR) in Liverpool, England from April 22 to 25, 2008. The study found that carbohydrate fructose can increase uric acid. It indicated that fructose plays a key role in impaired glucose tolerance as well as in insulin resistance and hyperinsulinemia. It also found that purine-rich vegetables do not change uric acid levels.

Introduction: La résistance à l’insuline est un phénomène complexe, résultant à la fois de facteurs génétiques et environnementaux. Parmi ceux-ci, le fructose semble induire de nombreux troubles métaboliques. Le but de cette étude était d’étudier les effets du fructose chez des personnes présentant une prédisposition génétique au développement de troubles métaboliques, à savoir des individus avec histoire familiale de diabète sucré de type 2 (DiabFam). Patients et méthodes: Des jeunes hommes sains avec DiabFam (n=9) ou sans (témoins, n=5) ont été soumis à un régime riche en fructose (3,5 g/kg masse maigre/jour) durant 6 jours. La sensibilité à l’insuline (SI) a été mesurée par un clamp hyperinsulinémique euglycémique à 2 paliers (0,3 et 1 mU/kg/min). La SI hépatique à jeun était évaluée par l’indice [100 ÷ (production hépatique de glucose × [insuline])], et la SI musculaire par le taux de renouvellement du glucose à haute dose d’insuline. Les lipides intrahépatiques (IHCL) et intramusculaires ont été mesurés par résonance magnétique nucléaire. Résultats: Le fructose augmente (P < 0,05) les VLDL-triglycérides (TG) (Control : +55 %, 0,38±0,07 vs 0,57±0,09 ; DiabFam : +148 %, 0,47±0,06 vs 1,06±0,12 mmol/L) et IHCL (témoin : +62 %, 5,3±0,8 vs 8,9±2,3 ; DiabFam : +105 %, 8,5±1,7 vs 15,8±2,6 mmol/kg). Ces augmentations étaient plus marquées chez les DiabFam que les témoins (P < 0,05). Le fructose diminue la SI hépatique (témoins : –15 %, 6,1±0,5 vs 5,1±0,8, P=0,3 ; DiabFam : –10 %, 5,2±0,4 vs 4,5±0,3, P=0,01), et élève le taux de transaminases (témoins : +73 %, 17±1 vs 26±5, P =0,1 ; DiabFam : +89 %, 16±1 vs 31±6 U/L, P =0,01). La SI musculaire était plus basse et les lipides intramusculaires plus élevés chez les DiabFam (P < 0,05), mais n’ont pas été influencés par le fructose. Conclusion: Une supplémentation en fructose de 6 jours induit des altérations au niveau hépatique, aussi bien fonctionnelles que morphologiques. Les sujets avec histoire familiale de diabète sont plus susceptibles aux perturbations du métabolisme hépatique des lipides. [Copyright &y& Elsevier]

The article discusses research on the association of high fructose intake with increased risk of kidney stones. According to it, individuals in the highest quintiles of total fructose intake and free fructose intake pose high risk for kidney stones. It is advised that patients with neprolithiasis should not increase their intake of foods rich with fructose.

The article reports on a study suggesting that consumption of excess fructose and glucose can inactivate the sex hormone-binding globulin (SHBG) gene that controls the levels of sex steroids in the body. It states that the protein encoded by this gene is needed to regulate the levels of available testosterone and estrogen in an individual.