A recent study entitled “The human brain produces fructose from glucose” published in JCI Insight sought to examine whether peripheral hyperglycemia can drive intracerebral production of fructose through the polyol pathway [glucose –(aldose reductase)à sorbitol –(sorbitol dehydrogenase)à fructose] in an exploratory study. Researchers at Yale selected 4 male and 4 female participants (mean: age 28.8, BMI 23.4mg/k2, HbA1c 2.9%) to participate in the study. Following an overnight fast, each participant was given one IV catheter in one arm to draw labs and a second IV catheter in the other arm to administer 20% dextrose every 5-10 minutes to achieve and maintain plasma glucose of 12 mmol/l. Blood was collected at baseline and at 30, 60, 120, 180 and 240 minutes during the hyperglycemic trial and 1H MRS spectrometer scans were used to measure intracerebral concentrations of fructose and glucose at the same time points.
As expected, plasma glucose rapidly increased during the dextrose infusion. Plasma fructose levels were only significantly greater than baseline after 180 minutes and 240 minutes of dextrose infusion. There were no differences in plasma sorbitol levels during the entire hyperglycemic clamping trial.
Intracerebral glucose levels rose significantly over time, beginning at 10 minutes after infusion initiation. Similarly, intracerebral fructose levels rose significantly overtime beginning at 20 minutes after infusion initiation. Intracerebral sorbitol was not measured. The magnitude of the change for intracerebral fructose was approximately 30% that of the change of intracerebral glucose.
Because intracerebral fructose concentrations levels rose more rapidly than plasma (20 minutes versus 180 minutes), researchers conclude that the increase in brain fructose is not a result of peripheral fructose crossing the blood brain barrier but is rather created endogenously from glucose through the polyol pathway.
Points of Consideration
o Furthermore researcher were unable to confirm that the observed results were a direct result of the polyol pathway. In rodent studies, this mechanism was demonstrated by administering sorbinil, an inhibitor of the rate limiting enzyme (aldose reductase), and observing subsequent decrease in the production of sorbitol and fructose following glucose administration.
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