Dietary fructose consumption among US children and adults: the Third National Health and Nutrition Examination Survey.
ABSTRACT High fructose intake has been associated with increased de novo lipogenesis in the liver as well as increased plasma triglycerides, insulin resistance, and obesity. Fructose occurs naturally in fruits and vegetables; however, it is added to many processed foods as table sugar (sucrose) and high-fructose corn syrup. Dietary data from a nationally representative sample in 1977-1978 estimated that mean consumption of fructose was 37 g/day (8% of total intake). Little is known about more recent fructose consumption patterns.
We determined the amount and sources of dietary fructose among US adults and children.
We examined fructose consumption patterns by sex, age group, race/ethnicity, socioeconomic status, and body mass index for 21,483 children and adults. We used a single 24-hour dietary recall administered in the third National Health and Examination Survey (NHANES).
Weighted estimates of fructose intake were tested for significant differences (P < .05) between groups.
The mean consumption of fructose was estimated to be 54.7g/day (range, 38.4-72.8) and accounted for 10.2% of total caloric intake. Consumption was highest among adolescents (12-18 years) at 72.8 g/day (12.1% of total calories). One fourth of adolescents consumed at least 15% of calories from fructose. The largest source of fructose was sugar-sweetened beverages (30%) followed by grains (22%) and fruit or fruit juice (19%).
Over 10% of Americans' daily calories were from fructose. These results, when compared with a previous nationally representative study, suggest that fructose consumption has increased. Further research is needed to understand the impact of increased intake of fructose on human health.
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ABSTRACT: Nonalcoholic fatty-liver disease (NAFLD) prevalence is increasing worldwide, with the affected US population estimated near 30%. Diet is a recognized risk factor in the NAFLD spectrum, which includes non-alcoholic steatohepatitis (NASH) and fibrosis. Low hepatic copper (Cu) was recently linked to clinical NAFLD/NASH severity. Simple sugar consumption including sucrose and fructose is implicated in NAFLD, while consumption of these macronutrients also decrease liver Cu levels. Though dietary sugar and low Cu are implicated in NAFLD, transcript-level responses that connect diet and pathology are not established. We have developed a mature rat model of NAFLD induced by dietary Cu deficiency, human-relevant high sucrose intake (30% w/w), or both factors in combination. Compared to the control diet with adequate Cu and 10% (w/w) sucrose, rats fed either high sucrose or low Cu diets had increased hepatic expression of genes involved in inflammation and fibrogenesis, including hepatic stellate cell activation, while the combination of diet factors also increased ATP citrate lyase (Acly) and fatty-acid synthase (Fasn) gene transcription (Fold change >2, p <0.02). Low dietary Cu decreased hepatic and serum Cu (p ≤0.05), promoted lipid peroxidation, and induced NAFLD-like histopathology, while the combined factors also induced fasting hepatic insulin resistance and liver damage. Neither low Cu nor 30% sucrose in the diet led to enhanced weight gain. Taken together, transcript profiles, histological and biochemical data indicate that low Cu and high sucrose promote hepatic gene expression and physiological responses associated with NAFLD and NASH, even in the absence of obesity or severe steatosis.
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ABSTRACT: ScopeThis study evaluated the capacity of dietary catechin (C), quercetin (Q), and the combination of both (CQ), to attenuate adipose inflammation triggered by high fructose (HFr) consumption in rats and by tumor necrosis factor alpha (TNF-α) in 3T3-L1 adipocytes.Methods and resultsIn rats, HFr consumption for 6 wk caused dyslipidemia, insulin resistance, reduced plasma adiponectin, adiposity, and adipose tissue inflammation. Dietary supplementation with 20 mg/kg/day of C, Q, and CQ improved all these parameters. In 3T3-L1 adipocytes, C and Q attenuated TNF-α-induced elevated protein carbonyls, increased proinflammatory cytokine expression (MCP-1, resistin), and decreased adiponectin. The protective effects of C and Q on adipose inflammation are in part associated with their capacity to (i) decrease the activation of the mitogen-activated kinases (MAPKs) JNK and p38; and (ii) prevent the downregulation of PPAR-γ. In summary, C and Q, and to a larger extent the combination of both, attenuated adipose proinflammatory signaling cascades and regulated the balance of molecules that improve (adiponectin) or impair (TNF-α, MCP-1, resistin) insulin sensitivity.Conclusion Together, these findings suggest that dietary Q and C may have potential benefits in mitigating MetS-associated adipose inflammation, oxidative stress, and insulin resistance.Molecular Nutrition & Food Research 01/2015; 59(4). DOI:10.1002/mnfr.201400631 · 4.91 Impact Factor
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ABSTRACT: Recent evidence suggests that fructose consumption is associated with weight gain, fat deposition and impaired cognitive function. However it is unclear whether the detrimental effects are caused by fructose itself or by the concurrent increase in overall energy intake. In the present study we examine the impact of a fructose diet relative to an isocaloric glucose diet in the absence of overfeeding, using a mouse model that mimics fructose intake in the top percentile of the USA population (18% energy). Following 77 days of supplementation, changes in body weight (BW), body fat, physical activity, cognitive performance and adult hippocampal neurogenesis were assessed. Despite the fact that no differences in calorie intake were observed between groups, the fructose animals displayed significantly increased BW, liver mass and fat mass in comparison to the glucose group. This was further accompanied by a significant reduction in physical activity in the fructose animals. Conversely, no differences were detected in hippocampal neurogenesis and cognitive/motor performance as measured by object recognition, fear conditioning and rotorod tasks. The present study suggests that fructose per se, in the absence of excess energy intake, increases fat deposition and BW potentially by reducing physical activity, without impacting hippocampal neurogenesis or cognitive function.Scientific Reports 04/2015; 5:9589. DOI:10.1038/srep09589 · 5.08 Impact Factor