Antiketogenic action of fructose, glyceraldehyde, and sorbitol in the rat in vivo.
The purpose of this study was to compare the metabolism and antiketogenic properties of fructose, glyceraldehyde, and sorbitol. Fructose, glyceraldehyde, and sorbitol were readily metabolized and exhibited an antiketogenic effect in both blood and liver when injected intramuscularly to starved (forty-eight hours) rats. Sorbitol had the most pronounced antiketogenic effect and produced an 80 to 90 per cent decrease in the blood ketone bodies sixty minutes after administration. Fructose and glyceraldehyde were equally effective and produced about a 60 to 70 per cent decrease in ketone bodies. Fructose, glyceraldehyde, and sorbitol caused a significant decrease in the concentration of hepatic ketone bodies. In liver, sorbitol was found to be most effective in its antiketogenic action. The concentration of plasma free fatty acids remained unchanged after injection of all three antiketogenic substrates. Fructose, glyceraldehyde, or sorbitol caused increased blood lactate and pyruvate concentrations, and fructose was the most effective of the three substrates. Fructose administration resulted in a significant decrease in hepatic lactate/pyruvate and beta-OH-butyrate/acetoacetate concentration ratios, whereas sorbitol caused an increase in the concentration ratio of these two substrat pairs. Decreases in blood and liver ketone body levels were associated with lowering of liver acetyl-CoA concentration . However, the decrease in hepatic acetyl-CoA produced upon the administration of antiketogenic substrates was not pronounced. Sorbitol administration resulted in the most pronounced increase in hepatic alpha-glycerophosphate concentration. Fructose or glyceraldehyde also caused an increase in alpha-glycerophosphate content. Administration of each of the three antiketogenic substrates produced an increase in hepatic dihydroxyacetone phosphate concentration. All three antiketogenic compounds increased liver glycogen and blood glucose concentrations. No significant changes were observed in hepatic ATP, ADP, or AMP concentrations sixty minutes after the injections of any of the antiketogenic substrates. Although decreased liver acetyl-CoA levels were associated with the antiketogenic effects of the compounds tested, the increased liver alpha-glycerophosphate content best explains the differences between fructose or glyceraldehyde and sorbitol.
D000105:Acetyl Coenzyme A / Q000378:metabolism; D000227:Adenine Nucleotides / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D004099:Dihydroxyacetone Phosphate / Q000378:metabolism; D005632:Fructose / Q000378:metabolism / Q000494:pharmacology*; D005985:Glyceraldehyde / Q000378:metabolism / Q000494:pharmacology*; D005994:Glycerophosphates / Q000378:metabolism; D007657:Ketone Bodies / Q000037:antagonists & inhibitors* / Q000378:metabolism; D007773:Lactates / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008112:Liver Glycogen / Q000378:metabolism; D008297:Male; D011773:Pyruvates / Q000378:metabolism; D051381:Rats; D013012:Sorbitol / Q000378:metabolism / Q000494:pharmacology*; D013217:Starvation
D000227:Adenine Nucleotides; D001786:Blood Glucose; D005994:Glycerophosphates; D007657:Ketone Bodies; D007773:Lactates; D008112:Liver Glycogen; D011773:Pyruvates; D005632:Fructose; D005985:Glyceraldehyde; D013012:Sorbitol; D004099:Dihydroxyacetone Phosphate; D000105:Acetyl Coenzyme A