Fructose

Capacity and rate of absorption
The absorption capacity for fructose in monosaccharide form ranges from less than 5 g to 50 g
and adapts with changes in dietary fructose intake. Studies show the greatest absorption rate
occurs when glucose and fructose are administered in equal quantities. When fructose is ingested
as part of the disaccharide sucrose, absorption capacity is much higher because fructose exists in
a 1:1 ratio with glucose. It appears that the GLUT5 transfer rate may be saturated at low levels,
and absorption is increased through joint absorption with glucose. One proposed mechanism for
this phenomenon is a glucose-dependent cotransport of fructose. In addition, fructose transfer
activity increases with dietary fructose intake. The presence of fructose in the lumen causes
increased mRNA transcription of GLUT5, leading to increased transport proteins. High-fructose
diets have been shown to increase abundance of transport proteins within 3 days of intake.
Malabsorption
Several studies have measured the intestinal absorption of fructose using hydrogen breath test.
These studies indicate that fructose is not completely absorbed in the small intestine. When
fructose is not absorbed in the small intestine, it is transported into the large intestine, where
it is fermented by the colonic flora. Hydrogen is produced during the fermentation process and
dissolves into the blood of the portal vein. This hydrogen is transported to the lungs, where it is
exchanged across the lungs and is measurable by the hydrogen breath test. The colonic flora also
produces carbon dioxide, short-chain fatty acids, organic acids, and trace gases in the presence
of unabsorbed fructose.. The presence of gases and organic acids in the large intestine causes
gastrointestinal symptoms such as bloating, diarrhea, flatulence, and gastrointestial pain Exercise
can exacerbate these symptoms by decreasing transit time in the small intestine, resulting in a
greater amount of fructose being emptied into the large intestine.
Fructose metabolism
DHAP can either be isomerized to glyceraldehyde 3-phosphate by triosephosphate isomerase
or undergo reduction to glycerol 3-phosphate by glycerol 3-phosphate dehydrogenase. The
glyceraldehyde produced may also be converted to glyceraldehyde 3-phosphate by glyceraldehyde
kinase or converted to glycerol 3-phosphate by glyceraldehyde 3-phosphate dehydrogenase. The
metabolism of fructose at this point yields intermediates in the gluconeogenic and fructolytic
pathways leading to glycogen synthesis as well as fatty acid and triglyceride synthesis.
Synthesis of glycogen from DHAP and glyceraldehyde 3 phosphate
The resultant glyceraldehyde formed by aldolase B then undergoes phosphorylation to
glyceraldehyde 3-phosphate. Increased concentrations of DHAP and glyceraldehyde 3-phosphate
in the liver drive the gluconeogenic pathway toward glucose and subsequent glycogen synthesis.
It appears that fructose is a better substrate for glycogen synthesis than glucose and that glycogen
replenishment takes precedence over triglyceride formation. Once liver glycogen is replenished,
the intermediates of fructose metabolism are primarily directed toward triglyceride synthesis.
All three dietary monosaccharides are transported into the liver by the GLUT 2 transporter. Fructose
and galactose are phosphorylated in the liver by fructokinase (Km= 0.5 mM) and galactokinase
(Km = 0.8 mM). By contrast, glucose tends to pass through the liver (Km of hepatic glucokinase
= 10 mM) and can be metabolised anywhere in the body. Uptake of fructose by the liver is not
regulated by insulin.
Fructolysis
Fructolysis initially produces fructose 1,6-bisphosphate, which is split to produce phosphate
derivatives of the trioses dihydroxyacetone and glyceraldehyde. These are then metabolized
either in the gluconeogenic pathway for glycogen replenishment and/or complete metabolism in
the fructolytic pathway to pyruvate, which after conversion to acetyl-CoA enters the Krebs cycle,
and is converted to citrate and subsequently directed toward ’’de novo’’ synthesis of the free fatty
acid palmitate.
Metabolism of fructose to DHAP and glyceraldehyde
Figure 6: Metabolic conversion of fructose to glycogen in the liver.
Synthesis of triglyceride from DHAP and glyceraldehyde 3 phosphate
The first step in the metabolism of fructose is the phosphorylation of fructose to fructose
1-phosphate by fructokinase, thus trapping fructose for metabolism in the liver. Fructose
1-phosphate then undergoes hydrolysis by aldolase B to form DHAP and glyceraldehydes;
Carbons from dietary fructose are found in both the free fatty acid and glycerol moieties of
plasma triglycerides. Processed High fructose mineral free consumption can lead to excess
pyruvate production, causing a buildup of Krebs cycle intermediates. Accumulated citrate can
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