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Absorption and metabolism of fructose by rat jejunum.

ABSTRACT: The absorption and metabolism of fructose was investigated in the vascularly perfused jejunum of fructose-fed rats. With 10 mM-glutamate and 10 mM-fructose in the lumen, the viability of the tissue is maintained and fructose is absorbed and utilized at high rates. With 28 mM-fructose in the lumen, glucose appears in the vascular bed. With 10 mM- or 28 mM-fructose in the presence of 10 mM- or mM-glucose in the lumen, the fructose absorption is decreased. From 10 mM- or 28 mM-sucrose in the lumen, fructose uptake is also less than from the equivalent concentration of free fructose. The rate of appearance of fructose in the vascular bed is independent of the source of fructose from which it is derived. In the presence of glucose, either free or as sucrose, there is a marked decrease in the utilization of fructose, defined as the difference between that absorbed by the jejunum and that transported unchanged into the vascular bed. In all cases about half of the carbohydrate absorbed from the lumen is converted into lactate, most of which is secreted into the blood. The absorption of glucose and the rate of vascular appearance of glucose from glucose in the lumen are about 1.5 times greater than those of fructose from fructose in the lumen. It is concluded: firstly, that fructose uptake from the lumen of rat jejunum is determined by its concentration and by the demand for it as a fuel for the intestine, a demand that is severely decreased in the presence of glucose; secondly, that in the vascularly perfused jejunum there is no evident kinetic advantage for uptake of fructose or glucose from sucrose rather than from free monosaccharide in the lumen; thirdly, that some fructose can be converted into glucose.

SUBMITTER: Holloway PA

PROVIDER: S-EPMC1144143 | biostudies-other | 1984 Aug

REPOSITORIES: biostudies-other

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Project description:Fructose reacts spontaneously with proteins in the brain to form advanced glycation end products (AGE) that may elicit neuroinflammation and cause brain pathology, including Alzheimer's disease. We investigated whether fructose is eliminated by oxidative metabolism in neocortex. Injection of [(14) C]fructose or its AGE-prone metabolite [(14) C]glyceraldehyde into rat neocortex in vivo led to formation of (14) C-labeled alanine, glutamate, aspartate, GABA, and glutamine. In isolated neocortical nerve terminals, [(14) C]fructose-labeled glutamate, GABA, and aspartate, indicating uptake of fructose into nerve terminals and oxidative fructose metabolism in these structures. This was supported by high expression of hexokinase 1, which channels fructose into glycolysis, and whose activity was similar with fructose or glucose as substrates. By contrast, the fructose-specific ketohexokinase was weakly expressed. The fructose transporter Glut5 was expressed at only 4% of the level of neuronal glucose transporter Glut3, suggesting transport across plasma membranes of brain cells as the limiting factor in removal of extracellular fructose. The genes encoding aldose reductase and sorbitol dehydrogenase, enzymes of the polyol pathway that forms glucose from fructose, were expressed in rat neocortex. These results point to fructose being transported into neocortical cells, including nerve terminals, and that it is metabolized and thereby detoxified primarily through hexokinase activity. We asked how the brain handles fructose, which may react spontaneously with proteins to form 'advanced glycation end products' and trigger inflammation. Neocortical cells took up and metabolized extracellular fructose oxidatively in vivo, and isolated nerve terminals did so in vitro. The low expression of fructose transporter Glut5 limited uptake of extracellular fructose. Hexokinase was a main pathway for fructose metabolism, but ketohexokinase (which leads to glyceraldehyde formation) was expressed too. Neocortical cells also took up and metabolized glyceraldehyde oxidatively.

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Absorption and metabolism of fructose by rat jejunum.

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