Effects of Dietary Fructose on Plasma Glucose and Hormone Responses in Normal and Hyperinsulinemic Men

Hallfrisch, Judith; Ellwood, Kathleen C.; Michaelis, Otho E.; Reiser, Sheldon; O'Dorisio, Thomas M.; Prather, Elizabeth S.

doi:10.1093/jn/113.9.1819

Cited by 108 publications

(70 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…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.

240

293

View full text Add to dashboard Cite

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

show abstract

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.

240

293

View full text Add to dashboard Cite

show abstract

“…Indeed, supply of fructose together with glucose was shown to increase glycogen synthesis by liver in the rat and dog (32,33). Although fructose can be efficient to relieve hyperglycemia in diabetes, the use of fructose as a substituent for glucose for diabetes patients has raised the controversy (34,35). F1P is effective for releasing GK from GKRP, but a high amount or long-term supply of fructose might result in unexpected loss of GK as a result of proteasomal degradation of free GK in cytosol (29), which can cause the hyperglycemia to be more serious.…”

Section: Discussionmentioning

confidence: 99%

Molecular basis for the role of glucokinase regulatory protein as the allosteric switch for glucokinase

Choi¹,

Seo²,

Kyeong³

et al. 2013

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

View full text Add to dashboard Cite

Glucokinase (GK) is a monomeric allosteric enzyme and plays a pivotal role in blood glucose homeostasis. GK is regulated by GK regulatory protein (GKRP), and indirectly by allosteric effectors of GKRP. Despite the critical roles of GK and GKRP, the molecular basis for the allosteric regulation mechanism of GK by GKRP remains unclear. We determined the crystal structure of Xenopus GK and GKRP complex in the presence of fructose-6-phosphate at 2.9 Å. GKRP binds to a super-open conformation of GK mainly through hydrophobic interaction, inhibiting the GK activity by locking a small domain of GK. We demonstrate the molecular mechanism for the modulation of GK activity by allosteric effectors of GKRP. Importantly, GKRP releases GK in a sigmoidal manner in response to glucose concentration by restricting a structural rearrangement of the GK small domain via a single ion pair. We find that GKRP acts as an allosteric switch for GK in blood glucose control by the liver.hexokinase | sigmoidicity I conformational restriction | type 2 diabetes

show abstract

“…In humans, the metabolic effect of increased fructose intake is not clear (Elliott et al, 2002). Hallfrisch et al (1983) have found that a diet containing 15% of energy as fructose has detrimental effects on glucose metabolism both in normal and hyperinsulinemic men. Reduced insulin sensitivity and insulin binding to its receptors has also been reported (BeckNielsen et al, 1980).…”

Section: Discussionmentioning

confidence: 99%

Impact of sugar beet pectin and polydextrose on fasting and postprandial glycemia and fasting concentrations of serum total and lipoprotein lipids in middle-aged subjects with abnormal glucose metabolism

Schwab

Louheranta

Törrönen³

et al. 2006

Eur J Clin Nutr

View full text Add to dashboard Cite

Objective: To examine the effects of sugar beet pectin (SBP) and polydextrose (PDX) on fasting plasma glucose concentration, serum lipid profile and postprandial glycemia in middle-aged subjects with abnormal glucose metabolism. Design: A placebo-controlled, randomized, parallel double-blinded study. Subjects and setting: Subjects were recruited via newspaper announcements. Seventy subjects were recruited of which 66 completed the study. Intervention: The intervention period lasted for 12 weeks during which the subjects consumed a drink enriched with either SBP (n ¼ 22) or PDX (n ¼ 22) or without fiber enrichment (control group, n ¼ 22). The daily dose of the drinks was 4 dl. The subjects were also given nutrition counseling. Postprandial glycemia was examined in 24 subjects (n ¼ 8 in each group) at 0 and 12 weeks after a standardized breakfast. Results: Fasting plasma glucose concentration did not change in the SBP and PDX groups, whereas it increased in the control group (P ¼ 0.007). On the contrary, the glycosylated hemoglobin A1 c increased marginally but significantly (Pp0.05) in the intervention groups without a change in the control group. In postprandial glycemia, no differences between the groups were found. In both the SBP and PDX groups, fasting serum High-density lipoprotein (HDL)-cholesterol concentration increased (Pp0.05) without a change in the control group. Total to HDL-cholesterol ratio decreased in all groups (Pp0.05). Conclusions: It was found that SBP and PDX do not have positive effects on fasting or postprandial plasma glucose concentrations or serum lipid profile in subjects with abnormal glucose metabolism. Sponsorship:

show abstract

Effects of Dietary Fructose on Plasma Glucose and Hormone Responses in Normal and Hyperinsulinemic Men

Cited by 108 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

Molecular basis for the role of glucokinase regulatory protein as the allosteric switch for glucokinase

Impact of sugar beet pectin and polydextrose on fasting and postprandial glycemia and fasting concentrations of serum total and lipoprotein lipids in middle-aged subjects with abnormal glucose metabolism

Contact Info

Product

Resources

About