Johnson RJ, Segal MS, Sautin Y, Nakagawa T, Feig DI, Kang DH 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: 6.77). 11/2007; 86(4):899-906.
Source: PubMed


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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Available from: Laura Gabriela Sánchez-Lozada,
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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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    • "High fructose intake has been associated with increased risk of metabolic syndrome, hypertension and elevated triglycerides. However, the potential impact of fructose on the stimulation of uric acid production has attracted the most attention, and is hypothesised to have a key role for inducing cardiorenal disease (Johnson et al., 2007). Experimental studies have identified a causal effect of fructose consumption on the development of features of the metabolic syndrome (Nakagawa et al., 2006), in addition to the deterioration of renal function, increased glomerulosclerosis and proteinuria in rats fed a high fructose diet (Teff et al., 2004). "
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    ABSTRACT: Dietary modification has long been considered a modifiable risk factor for the progression of chronic kidney disease (CKD) and a key management strategy in end-stage kidney disease. This review will focus on the history of the reoccurring focus on dietary components of salt and protein, as well as the impact of consumer behaviour moving towards convenience foods, on intake of phosphate and sugar in the form of fructose. The latest evidence in CKD supports diets low in sodium, discourages strict diets low in protein and presents a strong case to turn the cycle of eating habits back to basics, in a bid to lower processed food intake and improve the health outcomes of our CKD patients.
    Renal Society of Australasia Journal 11/2014; 10(3).
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