Article

High fructose corn syrup and diabetes prevalence: A global perspective

a Department of Preventive Medicine , University of Southern California , Los Angeles , CA , USA.
Global Public Health (Impact Factor: 0.92). 11/2012; 8(1). DOI: 10.1080/17441692.2012.736257
Source: PubMed

ABSTRACT Abstract The overall aim of this study was to evaluate, from a global and ecological perspective, the relationships between availability of high fructose corn syrup (HFCS) and prevalence of type 2 diabetes. Using published resources, country-level estimates (n=43 countries) were obtained for: total sugar, HFCS and total calorie availability, obesity, two separate prevalence estimates for diabetes, prevalence estimate for impaired glucose tolerance and fasting plasma glucose. Pearson's correlations and partial correlations were conducted in order to explore associations between dietary availability and obesity and diabetes prevalence. Diabetes prevalence was 20% higher in countries with higher availability of HFCS compared to countries with low availability, and these differences were retained or strengthened after adjusting for country-level estimates of body mass index (BMI), population and gross domestic product (adjusted diabetes prevalence=8.0 vs. 6.7%, p=0.03; fasting plasma glucose=5.34 vs. 5.22 mmol/L, p=0.03) despite similarities in obesity and total sugar and calorie availability. These results suggest that countries with higher availability of HFCS have a higher prevalence of type 2 diabetes independent of obesity.

Download full-text

Full-text

Available from: Michael I Goran, Feb 28, 2014
4 Followers
 · 
408 Views
  • Source
    • "In addition to HFD, high-sugar diets such as high fructose and sucrose have been more recently recognized as a potential risk of metabolic syndrome and diabetes independent of energy intake (Abdelmalek et al. 2012; Goran et al. 2013). A recent global study revealed that the consumption of high-fructose corn syrup explains a remarkable 20 % increase in T2D incidents [12]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Type 2 diabetes (T2D) has become an increasingly challenging health burden due to its high morbidity, mortality, and heightened prevalence worldwide. Although dietary and nutritional imbalances have long been recognized as key risk factors for T2D, the underlying mechanisms remain unclear. The advent of nutritional systems biology, a field that aims to elucidate the interactions between dietary nutrients and endogenous molecular entities in disease-related tissues, offers unique opportunities to unravel the complex mechanisms underlying the health-modifying capacities of nutritional molecules. The recent revolutionary advances in omics technologies have particularly empowered this incipient field. In this review, we discuss the applications of multi-omics approaches toward a systems-level understanding of how dietary patterns and particular nutrients modulate the risk of T2D. We focus on nutritional studies utilizing transcriptomics, epigenomomics, proteomics, metabolomics, and microbiomics, and integration of diverse omics technologies. We also summarize the potential molecular mechanisms through which nutritional imbalances contribute to T2D pathogenesis based on these studies. Finally, we discuss the remaining challenges of nutritional systems biology and how the field can be optimized to further our understanding of T2D and guide disease management via nutritional interventions.
    Genes & Nutrition 09/2015; 10(5):481. DOI:10.1007/s12263-015-0481-3 · 3.42 Impact Factor
    • "Women with gestational diabetes are at increased risk of development of complications, such as pre-eclampsia during pregnancy and cardiovascular disease later in life (Rich-Edwards et al. 2014). A similar adverse effect of high fructose intake during pregnancy could compromise both the mother and long-term metabolic health of her offspring (Goran et al. 2013). Maternal fructose intake through pregnancy has no effect on fetal weight or postnatal growth, although plasma insulin is modestly reduced (Vickers et al. 2011), but the longer-term responses to fructose feeding during reproduction have only been examined during lactation (Alzamendi et al. 2010). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Maternal carbohydrate intake is one important determinant of fetal body composition, but whether increased exposure to individual sugars has long-term adverse effects on the offspring is not well established. Therefore, we examined the effect of fructose feeding on the mother, placenta, fetus and her offspring up to 6 months of life when they had been weaned onto a standard rodent diet and not exposed to additional fructose. Dams fed fructose were fatter, had raised plasma insulin and triglycerides from mid-gestation and higher glucose near term. Maternal resistance arteries showed changes in function that could negatively affect regulation of blood pressure and tissue perfusion in the mother and development of the fetus. Fructose feeding had no effect on placental weight or fetal metabolic profiles, but placental gene expression for the glucose transporter GLUT1 was reduced, whereas the abundance of sodium-dependent neutral amino acid transporter-2 was raised. Offspring born to fructose-fed and control dams were similar at birth and had similar post-weaning growth rates, and neither fat mass nor metabolic profiles were affected. In conclusion, raised fructose consumption during reproduction results in pronounced maternal metabolic and vascular effects, but no major detrimental metabolic effects were observed in offspring up to 6 months of age.
    Reproduction Fertility and Development 07/2015; DOI:10.1071/RD15119 · 2.58 Impact Factor
  • Source
    • "Increased and frequent consumption of diets rich in sucrose (table sugar) and/or high fructose corn syrup (sweetener used in confectionaries and many beverages) expose the body to high levels of glucose and fructose. The consumption of sugar and sweeteners has increased for the past 40 years and is thought to be associated with the development of obesity, type II diabetes and cardiovascular diseases (Bray 2004; Brown 2008; Goran et al. 2013; Johnson et al. 2007; Kmietowicz 2012; Sheludiakova et al. 2012). Much attention has been focused on fructose based on its reported effects of increasing circulating triglycerides , dyslipidemia, hyperuricemia, and obesity (Lustig 2010; Tappy and Le 2010). "
    [Show abstract] [Hide abstract]
    ABSTRACT: The development of obesity is becoming an international problem and the role of fructose is unclear. Studies using liver tissue and hepatocytes have contributed to the understanding of fructose metabolism. Excess fructose consumption also affects extra hepatic tissues including adipose tissue. The effects of fructose on human adipocytes are not yet fully characterized, although in vivo studies have noted increased adiposity and weight gain in response to fructose sweetened-beverages. In order to understand and predict the metabolic responses of adipocytes to fructose, this study examined differentiating and differentiated human adipocytes in culture, exposed to a range of fructose concentrations equivalent to that reported in blood after consuming fructose. A stable isotope based dynamic profiling method using [U-13C6]-D-fructose tracer was used to examine the metabolism and fate of fructose. A targeted stable isotope tracer fate association method was used to analyze metabolic fluxes and flux surrogates with exposure to escalating fructose concentration. This study demonstrated that fructose stimulates anabolic processes in adipocytes robustly, including glutamate and de novo fatty acid synthesis. Furthermore, fructose also augments the release of free palmitate from fully differentiated adipocytes. These results imply that in the presence of fructose, the metabolic response of adipocytes in culture is altered in a dose dependent manner, particularly favoring increased glutamate and fatty acid synthesis and release, warranting further in vivo studies.
    Metabolomics 06/2015; DOI:10.1007/s11306-014-0716-0 · 3.97 Impact Factor
Show more