Conversion of fructose to glucose in the rabbit small intestine. A reappraisal of the direct pathway (original) (raw)
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FRUCTOSE metabolism in the liver
Nutrition reviews, 1954
I would like to take this opportunity to e:q)ress. my sincere thanks to Professor J.B. Pridham for his encouragement and guidance during the supervision of this work. I wish to thank Professor I. MacDonald of the Physiology Department of Guy's Hospital Medical School for the interest taken in this work and for his helpful discussions. J also wish to express my gratitude to Dr. K. Clarke and Mr. D. Davies for their most helpful discussions and assistance in the earlier stages of this project. I am Indebted to Rank Hovis McDougall for financial assistance, It is impossible to acknowledge individually the large number of people who have helped in a more limited fashion to make this thesis possible. However, I would like to take this opportunity to thank them collectively. Finally to my wife Wendy I would add, "Your encouragement and assistance when the going was hard is no small contribution to this work, the least I can say is that I hope to reply in kind one day, until then, and even then, I will always be grateful".-i.e.
Influence of feeding fructose on fructose and glucose absorption in rat jejunum and ileum
Research in Experimental Medicine, 1981
The influence of feeding isocaloric diets containing either 65% of fructose (F 65) or 65% of glucose (G 65) were studied on the uptake of both sugars in segments of rat proximal jejunum and distal ileum. The hexose absorption was compared to that obtained in animals receiving isocaloric amounts of a diet containing 30% of glucose (G 30). Feeding fructose (F 65) for 3 days resulted in a 2.5-fold increase of fructose uptake in the jejunum and a 40% increase in the ileum as compared to group G30. When fructose (F65) was administered instead of G 65 the uptake of fructose was enhanced by 75% in the jejunum and 35% in the ileum. Stimulation of glucose absorption in segments of the proximal and distal small intestine by diets F 65 and G 65 was nearly identical as compared to the values of group G 30. The stimulation of the uptake of fructose induced by fructose feeding parallels an adaptive increase in the activity of enzymes involved in fructose metabolism in the mucosa of the small intestine.
Archives of Biochemistry and Biophysics, 2002
The metabolism of D D -glucose and/or D D -fructose was investigated in pancreatic islets from control rats and hereditarily diabetic GK rats. In the case of both D D -glucose and D D -fructose metabolism, a preferential alteration of oxidative events was observed in islets from GK rats. The generation of 3 HOH from D D -[5-3 H]glucose (or D D -[5-3 H]fructose) exceeded that from D D -[3-3 H]glucose (or D D -[3-3 H]fructose) in both control and GK rats. This difference, which is possibly attributable to a partial escape from glycolysis of tritiated dihydroxyacetone phosphate, was accentuated whenever the rate of glycolysis was decreased, e.g., in the absence of extracellular Ca 2þ or presence of exogenous D D -glyceraldehyde. D D -Mannoheptulose, which inhibited D D -glucose metabolism, exerted only limited effects upon D D -fructose metabolism. In the presence of both hexoses, the paired ratio between D D -[U-14 C]fructose oxidation and D D -[3-3 H]fructose or D D -[5-3 H]fructose utilization was considerably increased, this being probably attributable, in part at least, to a preferential stimulation by the aldohexose of mitochondrial oxidative events. Moreover, this coincided with the fact that D D -mannoheptulose now severely inhibited the catabolism of D D -[5-3 H]fructose and D D -[U-14 C]
Mini review on fructose metabolism
Obesity Research & Clinical Practice, 2013
Fructose is a monosaccharide and reducing sugar. It is present in sucrose and honey. Researchers around the world have come together in a just-published study that offers new ideas about how fructose consumption results in obesity and metabolic syndrome, which can lead to diabetes. In this review, we discuss that how fructose causes fatty liver, obesity and insulin resistance. We also discuss the effects of consumption of high fructose corn syrup, dietary fructose, fructoseinduced changes in metabolism.
American journal of physiology. Gastrointestinal and liver physiology, 2015
Elevated blood fructose concentrations constitute the basis for organ dysfunction in fructose-induced metabolic syndrome. We hypothesized that diet-induced changes in blood fructose concentrations are regulated by ketohexokinase (KHK) and the fructose transporter GLUT5. Portal and systemic fructose concentrations determined by HPLC in wildtype mice fed for 7 d 0% free fructose were <0.07 mM, were independent of time after feeding, were similar to those of GLUT5-/-, and did not lead to hyperglycemia. Postprandial fructose levels however increased markedly in those fed isocaloric 20% fructose, causing significant hyperglycemia. Deletion of KHK prevented fructose-induced hyperglycemia, but caused dramatic hyperfructosemia (>1 mM) with reversed portal to systemic gradients. Systemic fructose in wildtype and KHK-/- changed by 0.34 and 1.8 mM, respectively, for every mM increase in portal fructose concentration. Systemic glucose varied strongly with systemic, but not portal, fructos...
Nutrition & Metabolism, 2013
Whether dietary fructose (as sucrose or high fructose corn syrup) has unique effects separate from its role as carbohydrate, or, in fact, whether it can be considered inherently harmful, even a toxin, has assumed prominence in nutrition. Much of the popular and scientific media have already decided against fructose and calls for regulation and taxation come from many quarters. There are conflicting data, however. Outcomes attributed to fructoseobesity, high triglycerides and other features of metabolic syndromeare not found in every experimental test and may be more reliably caused by increased total carbohydrate. In this review, we try to put fructose in perspective by looking at the basic metabolic reactions. We conclude that fructose is best understood as part of carbohydrate metabolism. The pathways of fructose and glucose metabolism converge at the level of the triosephosphates and, therefore, any downstream effects also occur with glucose. In addition, a substantial part of ingested fructose is turned to glucose. Regulation of fructose metabolism per se, is at the level of substrate controlthe lower K m of fructokinase compared to glucokinase will affect the population of triose-phosphates. Generally deleterious effects of administering fructose alone suggest that fructose metabolism is normally controlled in part by glucose. Because the mechanisms of fructose effects are largely those of a carbohydrate, one has to ask what the proper control should be for experiments that compare fructose to glucose. In fact, there is a large literature showing benefits in replacing total carbohydrate with other nutrients, usually fat, and such experiments sensibly constitute the proper control for comparisons of the two sugars. In terms of public health, a rush to judgement analogous to the fat-cholesterol-heart story, is likely to have unpredictable outcome and unintended consequences. Popular opinion cannot be ignored in this problem and comparing fructose to ethanol, for example, is without biochemical correlates. Also, nothing in the biochemistry suggests that sugar is a toxin. Dietary carbohydrate restriction remains the best strategy for obesity, diabetes and metabolic syndrome. The specific contribution of the removal of fructose or sucrose to this effect remains unknown.
Small amounts of fructose markedly augment net hepatic glucose uptake in the conscious dog
Diabetes, 1998
Fructose activates glucokinase by releasing the enzyme from its inhibitory protein in liver. To examine the importance of acute activation of glucokinase in regulating hepatic glucose uptake, the effect of intraportal infusion of a small amount of fructose on net hepatic glucose uptake (NHGU) was examined in 42 h-fasted conscious dogs. Isotopic ([3-3H] and [U-14C]glucose) and arteriovenous difference methods were used. Each study consisted of an equilibration period (-90 to -30 min), a control period (-30 to 0 min), and a hyperglycemic/hyperinsulinemic period (0-390 min). During the latter period, somatostatin (489 pmol x kg(-1) x min(-1)) was given, along with intraportal insulin (7.2 pmol x kg(-1) x min(-1)) and glucagon (0.5 ng x kg(-1) x min(-1)). In this way, the liver sinusoidal insulin level was fixed at four times basal (456 +/- 60 pmol/l), and liver sinusoidal glucagon level was kept basal (46 +/- 6 ng/l). Glucose was infused through a peripheral vein to create hyperglycemi...
Proceedings of the National Academy of Sciences, 1990
An inborn deficiency in the ability of aldolase B to split fructose 1-phosphate is found in humans with hereditary fructose intolerance (HFI). A stable isotope procedure to elucidate the mechanism of conversion of fructose to glucose in normal children and in HFI children has been developed. A constant infusion of D-[U-'3C]fructose was given nasogastrically to control and to HFI children. Hepatic fructose conversion to glucose was estimated by examination of 13C NMR spectra of plasma glucose. The conversion parameters in the control and HFI children were estimated on the basis of doublet/singlet values of the plasma 13-glucose C-1 splitting pattern as a function of the rate of fructose infusion (0.26-0.5
Magnetic Resonance in Medicine, 2020
The pentose phosphate pathway (PPP) is an important component of hepatic intermediary metabolism. Jin et al. developed an elegant 13 C-NMR method for measuring hepatic PPP flux by quantifying the distribution of glucose 13 C-isotopomers formed from [U-13 C]glycerol. We demonstrate that this approach can be extended to exogenous [U-13 C]fructose and [U-13 C]glucose precursors by 13 C-NMR analysis of glycogen. Methods: Twelve male C57BL/6 mice fed standard chow were provided a 55/45 mixture of fructose and glucose at 30% w/v in the drinking water for 18 weeks. On the evening before sacrifice, the fructose component was enriched with 20% [U-13 C]fructose for 6 mice while the glucose component was enriched with 20% [U-13 C]glucose for the remaining 6 mice. Mice were allowed to feed and drink naturally overnight and then euthanized. Livers were freeze-clamped and glycogen was extracted and derivatized for 13 C NMR spectroscopy. Flux of each sugar into the PPP relative to its incorporation into glycogen was quantified from selected 13 C glycogen isotopomer ratios. Results: Both [U-13 C]fructose and [U-13 C]glucose precursors yielded glycogen 13 C-isotopomer distributions that were characteristic of PPP activity. The fraction of [U-13 C]glucose utilized by the PPP relative to its conversion to glycogen via the direct pathway was 14±1% while that from [U-13 C]fructose relative to its conversion to glycogen via the indirect pathway was significantly lower (10±1%, p=0.00032). Conclusions: Hepatic PPP fluxes from both [U-13 C]glucose and [U-13 C]fructose precursors were assessed by 13 C NMR analysis of glycogen 13 C-isotopomers. Glucose-6-phosphate generated via glucokinase and the direct pathway is preferentially utilized by the PPP.