A 4-wk high-fructose diet alters lipid metabolism without affecting insulin sensitivity or ectopic lipids in healthy humans

Lê, Kim-Anne; Faeh, David; Stettler, Rodrigue; Ith, Michael; Kreis, Roland; Vermathen, Peter; Boesch, Chris; Ravussin, Éric; Tappy, Luc

doi:10.1093/ajcn/84.6.1374

Cited by 252 publications

(146 citation statements)

References 36 publications

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“…Fructose absorption is also enhanced by prior exposure to fructose (31,32). This may explain why clinical studies investigating the effects of fructose on lipids and insulin resistance show greater metabolic effects of fructose on subjects who are overweight or insulin resistant or with a family history of diabetes (5,6,(33)(34)(35), as opposed to those that are healthy and lean (36,37). In addition, humans may be more predisposed to the metabolic effects of fructose because they do not synthesize vitamin C and also lack uricase, resulting in higher uric acid levels (38,39).…”

Section: Discussionmentioning

confidence: 99%

Opposing effects of fructokinase C and A isoforms on fructose-induced metabolic syndrome in mice

Ishimoto

Lanaspa²,

Le³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

249

293

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Fructose intake from added sugars correlates with the epidemic rise in obesity, metabolic syndrome, and nonalcoholic fatty liver disease. Fructose intake also causes features of metabolic syndrome in laboratory animals and humans. The first enzyme in fructose metabolism is fructokinase, which exists as two isoforms, A and C. Here we show that fructose-induced metabolic syndrome is prevented in mice lacking both isoforms but is exacerbated in mice lacking fructokinase A. Fructokinase C is expressed primarily in liver, intestine, and kidney and has high affinity for fructose, resulting in rapid metabolism and marked ATP depletion. In contrast, fructokinase A is widely distributed, has low affinity for fructose, and has less dramatic effects on ATP levels. By reducing the amount of fructose for metabolism in the liver, fructokinase A protects against fructokinase C-mediated metabolic syndrome. These studies provide insights into the mechanisms by which fructose causes obesity and metabolic syndrome.ketohexokinase | hepatic steatosis | insulin | leptin

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Section: Discussionmentioning

confidence: 99%

Opposing effects of fructokinase C and A isoforms on fructose-induced metabolic syndrome in mice

Ishimoto

Lanaspa²,

Le³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

249

293

View full text Add to dashboard Cite

show abstract

“…In this study, the subjects ingested a moderate amount of fructose (0.5 g/kg body weight). Although other studies have employed 0.75-1.5 g/kg of fructose 7,17) , these high amounts of fructose often induce malabsorption that causes gastrointestinal symptoms, for example bloating, abdominal pain and diarrhea [18][19][20] . HFCS-sweetened beverages contain approximately 20-30 g/500 mL of fructose 21) .…”

Section: Discussionmentioning

confidence: 99%

Simultaneous Ingestion of Fructose and Fat Exacerbates Postprandial Exogenous Lipidemia in Young Healthy Japanese Women

Saito

Kagaya

Suzuki

et al. 2013

JAT

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“…7). Given that the metabolic handling of fructose is similar in rats and humans, 42 and the fact that fructose administration as liquid solution to healthy male volunteers results in hyperleptinemia, 43 it is plausible that similar mechanisms may operate in humans, following excessive consumption of beverages containing fructose.…”

Section: Discussionmentioning

confidence: 99%

Suppressor of cytokine signaling-3 (SOCS-3) and a deficit of serine/threonine (Ser/Thr) phosphoproteins involved in leptin transduction mediate the effect of fructose on rat liver lipid metabolism

et al. 2008

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There is controversy regarding whether fructose in liquid beverages constitutes another dietary ingredient of high caloric density or introduces qualitative changes in energy metabolism that further facilitate the appearance of metabolic diseases. Central to this issue is the elucidation of the molecular mechanism responsible for the metabolic alterations induced by fructose ingestion. Fructose administration (10% wt/vol) in the drinking water of Sprague-Dawley male rats for 14 days induced hyperleptinemia and hepatic leptin resistance. This was caused by impairment of the leptin-signal transduction mediated by both janus-activated kinase-2 and the mitogen-activated protein kinase pathway. The subsequent increase in activity in the liver of the unphosphorylated and active form of the forkhead box O1 nuclear factor, which transrepresses peroxisome proliferator-activated receptor ␣ activity, and a lack of activation of the adenosine monophosphate-activated protein kinase, led to hypertriglyceridemia and hepatic steatosis. These alterations are attributable to two key events: (1) F ructose makes up a significant proportion of energy in westernized diets, mainly due to the high intake of fructose-containing beverages. This situation has coincided with the growing prevalence of obesity and metabolic syndrome, recognized risk factors for cardiovascular diseases, over the past two decades. 1,2 Fructose in liquid diets induces hypertriglyceridemia to a greater extent than in solid diets. 3 A 10% dietary energy increase in

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A 4-wk high-fructose diet alters lipid metabolism without affecting insulin sensitivity or ectopic lipids in healthy humans

Abstract: Moderate fructose supplementation over 4 wk increases plasma triacylglycerol and glucose concentrations without causing ectopic lipid deposition or insulin resistance in healthy humans.

Cited by 252 publications

References 36 publications

Opposing effects of fructokinase C and A isoforms on fructose-induced metabolic syndrome in mice

Opposing effects of fructokinase C and A isoforms on fructose-induced metabolic syndrome in mice

Simultaneous Ingestion of Fructose and Fat Exacerbates Postprandial Exogenous Lipidemia in Young Healthy Japanese Women

Suppressor of cytokine signaling-3 (SOCS-3) and a deficit of serine/threonine (Ser/Thr) phosphoproteins involved in leptin transduction mediate the effect of fructose on rat liver lipid metabolism

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