Pathways of Sugar and Alcohol Metabolism

Pathways of Sugar and Alcohol Metabolism: Fructose, Galactose, Pentose Phosphate Pathway, and Ethanol Metabolism:

• Fructose is ingested principally as the monosaccharide or as part of sucrose. Fructose metabolism generates fructose 1-phosphate, which is converted to intermediates of the glycolytic pathway.
• Galactose is ingested principally as lactose, which is converted to glucose and galactose in the intestine. Galactose metabolism generates first galactose 1-phosphate, which is converted to uridine diphosphate (UDPgalactose). The end product is glucose 1-phosphate, which is isomerized to glucose 6-phosphate, which enters glycolysis.
• The energy yield through glycolysis for both fructose and galactose is the same as for glucose metabolism.
• The pentose phosphate pathway consists of both oxidative and nonoxidative reactions.
• The oxidative steps of the pentose phosphate pathway generate NADPH and ribulose 5-phosphate from glucose 6-phosphate.
  • Ribulose 5-phosphate is converted to ribose 5-phosphate for nucleotide biosynthesis.
  • NADPH is utilized as reducing power for biosynthetic pathways.
• The nonoxidative steps of the pentose phosphate pathway reversibly convert five-carbon sugars to fructose 6-phosphate and glyceraldehyde 3-phosphate.
• Ethanol is metabolized to acetate primarily in the liver, generating NADH.
• The enzymes involved in ethanol metabolism are alcohol and aldehyde dehydrogenases.
• High or chronic ethanol ingestion induces a microsomal ethanol oxidizing system composed of cytochrome P450 enzymes in the endoplasmic reticulum.
• Acute effects of ethanol ingestion arise principally from the generation of NADH, which increases the NADH/NAD⁺ ratio of the liver. This leads to the following:
  • Inhibition of fatty acid oxidation
  • Inhibition of ketogenesis
  • Lactic acidosis
  • Hypoglycemia
• Long-term effects of ethanol are due to acetaldehyde and free-radical production, which leads to fatty liver, hepatitis, and liver cirrhosis.