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Johnson, R. J. et al. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. Am. J. Clin. Nutr. 86, 899-906

Division of Nephrology and Department of Medicine, University of Florida, Gainesville, FL, USA.
American Journal of Clinical Nutrition (Impact Factor: 6.92). 11/2007; 86(4):899-906.
Source: PubMed

ABSTRACT Currently, we are experiencing an epidemic of cardiorenal disease characterized by increasing rates of obesity, hypertension, the metabolic syndrome, type 2 diabetes, and kidney disease. Whereas excessive caloric intake and physical inactivity are likely important factors driving the obesity epidemic, it is important to consider additional mechanisms. We revisit an old hypothesis that sugar, particularly excessive fructose intake, has a critical role in the epidemic of cardiorenal disease. We also present evidence that the unique ability of fructose to induce an increase in uric acid may be a major mechanism by which fructose can cause cardiorenal disease. Finally, we suggest that high intakes of fructose in African Americans may explain their greater predisposition to develop cardiorenal disease, and we provide a list of testable predictions to evaluate this hypothesis.

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    • "Based on our research and theorizing, connecting a fast-food meal with spoonfuls of lard may help to reduce preference for these unhealthy, fatty meals. In terms of practical advancements, some studies indicate that the over-consumption of SSBs may pose a serious public-health threat (Belpoggi et al., 2006; Johnson et al., 2007; Ludwig et al., 2001; Schulze et al., 2004; but see Forshee et al., 2008; Gibson, 2008 "
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    • "Given the current worldwide shift toward a westernized lifestyle, there is an urgent need to address the relationship between the quality and quantity of nutrient intake during pregnancy and/or lactation and the metabolic fate of the offspring [5]. Fructose, present in added sugars such as sucrose and high-fructose corn syrup, has been linked to obesity and metabolic syndrome [6] [7] [8]. Experimental studies have shown that fructose can induce leptin resistance and features of metabolic syndrome in rats, whereas glucose intake does not [9] [10] [11]. "
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    ABSTRACT: Objective. Fructose intake from added sugars correlates with the epidemic rise in metabolic syndrome and cardiovascular diseases. However, consumption of beverages containing fructose is allowed during gestation. Recently, we found that an intake of fructose (10% wt/vol) throughout gestation produces an impaired fetal leptin signalling. Therefore, we have investigated whether maternal fructose intake produces subsequent changes in their progeny. Methods. Blood samples fromfed and 24 h fasted female andmale 90-day-old rats born fromfructose-fed, glucose-fed, or controlmothers were used. Results. After fasting,HOMA-IR and ISI (estimates of insulin sensitivity) were worse in male descendents fromfructose-fedmothers in comparison to the other two groups, and these findings were also accompanied by a higher leptinemia. Interestingly, plasma AOPP and uricemia (oxidative stress markers) were augmented in male rats from fructose-fed mothers compared to the animals from control or glucose-fed mothers. In contrast, female rats did not show any differences in leptinemia between the three groups. Further, insulin sensitivity was significantly improved in fasted female rats fromcarbohydrate-fed mothers. In addition, plasma AOPP levels tended to be diminished in female rats from carbohydrate-fed mothers. Conclusion.Maternal fructose intake induces insulin resistance, hyperleptinemia, and plasma oxidative stress in male, but not female, progeny.
    Journal of nutrition and metabolism 01/2015; 2015. DOI:10.1155/2015/158091
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    • "Over the past several decades the use of fructose, as a sweetener, has emerged in processed foods, soft drinks, and an assortment of desserts [1] [2] [3]. Fructose has been linked to the development and exacerbation of centripetal obesity and metabolic syndrome, in both animals and humans [3]. "
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    ABSTRACT: Background. Fructose metabolism is an unregulated metabolic pathway and excessive fructose consumption is known to activate ROS. HO-1 is a potent antioxidant gene that plays a key role in decreasing ROS and isoprostanes. We examined whether the fructose-mediated increase in adipocyte dysfunction involves an increase in isoprostanes and that pharmacological induction of HO-1 would decrease both isoprostane levels and adipogenesis. Methods and Results. We examined the effect of fructose, on adipogenesis in human MSCs in the presence and absence of CoPP, an inducer of HO-1. Fructose increased adipogenesis and the number of large lipid droplets while decreasing the number of small lipid droplets (). Levels of heme and isoprostane in fructose treated MSC-derived adipocytes were increased. CoPP reversed these effects and markedly increased HO-1 and the Wnt signaling pathway. The high fructose diet increased heme levels in adipose tissue and increased circulating isoprostane levels ( versus control). Fructose diets decreased HO-1 and adiponectin levels in adipose tissue. Induction of HO-1 by CoPP decreased isoprostane synthesis ( versus fructose). Conclusion. Fructose treatment resulted in increased isoprostane production and adipocyte dysfunction, which was reversed by the increased expression of HO-1.
    Journal of nutrition and metabolism 09/2014; DOI:10.1155/2014/980547
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