The Ingestion of a Fructose-Containing Beverage Combined with Fat Cream Exacerbates Postprandial Lipidemia in Young Healthy Women

Saito, Hiromi; Kato, Maiko; Yoshida, Akihiro; Naito, Michitaka

doi:10.5551/jat.22681

Cited by 17 publications

(10 citation statements)

References 24 publications

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“…In healthy volunteers, consumption of a high-fructose diet increases blood levels not only of glucose, triglycerides, and triglyceride-rich lipoproteins but also of ApoB48 (34, 131). In healthy women consuming 0.5-g/kg fructose (equivalent to about one can of regular soda) plus fat, similar results were observed in that fructose plus fat, but not fat alone, sharply raised postprandial levels of ApoB48 and of remnant-like particle triglycerides (110, 111). These fructose-induced increases in ApoB48 persisted even after fasting.…”

Section: Glut5 and Fructose-related Gastrointestinal Diseases And Synsupporting

confidence: 64%

“…In rats and mice, peripheral blood concentrations increase when fructose is consumed, and the increase is abolished if GLUT5 is deleted (4, 102). The magnitude of this increase is dependent on dietary fructose levels in both animal models (4, 102) and healthy human volunteers (77, 110, 111, 131). Urine fructose concentrations in mice also increased markedly with dietary fructose (38; M. Fukazawa, personal communication).…”

Section: Regulation Of Blood Fructose Levelsmentioning

confidence: 99%

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Intestinal Absorption of Fructose

2018

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Increased understanding of fructose metabolism, which begins with uptake via the intestine, is important because fructose now constitutes a physiologically significant portion of human diets and is associated with increased incidence of certain cancers and metabolic diseases. New insights in our knowledge of intestinal fructose absorption mediated by the facilitative glucose transporter GLUT5 in the apical membrane and by GLUT2 in the basolateral membrane are reviewed. We begin with studies related to structure as well as ligand binding, then revisit the controversial proposition that apical GLUT2 is the main mediator of intestinal fructose absorption. The review then describes how dietary fructose may be sensed by intestinal cells to affect the expression and activity of transporters and fructolytic enzymes, to interact with the transport of certain minerals and electrolytes, and to regulate portal and peripheral fructosemia and glycemia. Finally, it discusses the potential contributions of dietary fructose to gastrointestinal diseases and to the gut microbiome.

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Section: Glut5 and Fructose-related Gastrointestinal Diseases And Synsupporting

confidence: 64%

Section: Regulation Of Blood Fructose Levelsmentioning

confidence: 99%

Intestinal Absorption of Fructose

2018

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“…In our previous study, the postprandial lipidemia following the ingestion of fructose (0.5 g/kg body mass) in combination with fat cream (0.35 g/kg as fat) was higher than that following the ingestion of glucose [1]. The ingestion of a high-fructose syrup-containing beverage in combination with fat cream also delayed and exacerbated both exogenous and endogenous lipoprotein metabolism, and the ratio of fructose to glucose contained in the beverage was a key factor in the metabolic disturbance when the sugar load was equicaloric [2]. Practically, the ingestion of cola (a high-fructose beverage) in combination with a hamburger (a high-fat diet) was shown to delay postprandial lipidemia compared to the ingestion of a hamburger only, indicating that the fructose contained in the cola delayed and exacerbated postprandial lipidemia [3,4].…”

Section: Introductionmentioning

confidence: 95%

Effect of Ingesting Resistant Maltodextrin on Postprandial Hyperlipidemia Induced by Fructose in Young Women

Kuzawa¹,

Yoshida²,

Tsukamoto³

et al. 2019

JFNS

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Aim: Our previous study demonstrated that the ingestion of fructose with fat exacerbated and delayed postprandial lipid metabolism (J Atheroscler Thromb 2013; 20: 591). Herein, we investigated the effect of ingesting a water-soluble dietary fiber, resistant maltodextrin (RMD), which has been reported to be effective for ameliorating postprandial glycemia and lipidemia, on fructose-induced postprandial hyperlipidemia in healthy young women. Methods: Healthy young Japanese women with apolipoprotein E3/3 phenotype were enrolled. They underwent 4 test trials in a randomized crossover design: fat cream (0.35 g/kg of fat; F trial), fat cream with RMD (5 g; FR trial), fat cream with fructose (0.5 g/kg; FFr trial), and fat cream with fructose and RMD (FFrR trial). Blood samples were taken before (0) and at 0.5, 1, 2, 4, and 6 h after ingestion. Results: The serum glucose and insulin concentrations peaked at 0.5 h in the FFr and FFrR trials, and no difference was observed between these trials. There was no increase in glucose concentration in the F or FR trials. The serum triglyceride and apolipoprotein B48 concentrations peaked at 4 h in all trials. In the F and FR trials (but not in the FFr and FFrR trials), the serum triglyceride concentration returned to the fasting level at 6 h. In all trials, the apolipoprotein B48 concentration did not return to baseline at 6 h. Conclusion: Co-ingestion of RMD did not significantly inhibit fructose-induced postprandial hyperlipidemia.

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“…This was also associated with significantly higher serum TG and TRL remnant-like particle (RLP)-TG. A follow-up study by the same group, again using healthy Japanese females ( n = 12), varied the relative proportions of glucose and fructose ( w / w ) in the test meal (0.5 g/kg body weight), giving either 100% glucose or fructose (G100; F100), 90% fructose and 10% glucose (F90G10) or 55% fructose and 45% glucose (F55G45), in combination with the same amount of OFTT cream [84]. All drinks significantly increased plasma apoB48 levels at 2 and 4h post-prandially.…”

Section: Fructose Effects On Intestinal Lipoprotein Secretionmentioning

confidence: 99%

Role of the Enterocyte in Fructose-Induced Hypertriglyceridaemia

et al. 2017

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Dietary fructose has been linked to an increased post-prandial triglyceride (TG) level; which is an established independent risk factor for cardiovascular disease. Although much research has focused on the effects of fructose consumption on liver-derived very-low density lipoprotein (VLDL); emerging evidence also suggests that fructose may raise post-prandial TG levels by affecting the metabolism of enterocytes of the small intestine. Enterocytes have become well recognised for their ability to transiently store lipids following a meal and to thus control post-prandial TG levels according to the rate of chylomicron (CM) lipoprotein synthesis and secretion. The influence of fructose consumption on several aspects of enterocyte lipid metabolism are discussed; including de novo lipogenesis; apolipoprotein B48 and CM-TG production; based on the findings of animal and human isotopic tracer studies. Methodological issues affecting the interpretation of fructose studies conducted to date are highlighted; including the accurate separation of CM and VLDL. Although the available evidence to date is limited; disruption of enterocyte lipid metabolism may make a meaningful contribution to the hypertriglyceridaemia often associated with fructose consumption.

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The Ingestion of a Fructose-Containing Beverage Combined with Fat Cream Exacerbates Postprandial Lipidemia in Young Healthy Women

Cited by 17 publications

References 24 publications

Intestinal Absorption of Fructose

Intestinal Absorption of Fructose

Effect of Ingesting Resistant Maltodextrin on Postprandial Hyperlipidemia Induced by Fructose in Young Women

Role of the Enterocyte in Fructose-Induced Hypertriglyceridaemia

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