Metabolic alterations in cancer. Part I. Carbohydrate metabolism.
Glucose intolerance seen in weight-losing patients may not result from qualitative or quantitative alterations in insulin secretion or binding. It may, however, be the result of increased gluconeogenic flux which occurs in these patients. This may be due to increased substrate availability resulting from lactate production as the unoxidized-end-product of tumour glycolysis (Warburg effect). In addition, increased levels of glucogenic amino acid may be associated with preferential amino acid sequestration by the tumour, causing decreased muscle proteogenesis and therefore atrophy. Enhanced glucose demand by tumour cells may also lead to an increased hepatic gluconeogenesis, as will the production of ectopic ACTH.
D000105:Acetyl Coenzyme A / Q000378:metabolism; D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D005260:Female; D005943:Gluconeogenesis; D005947:Glucose / Q000378:metabolism*; D005951:Glucose Tolerance Test; D006801:Humans; D007003:Hypoglycemia / Q000150:complications; D007773:Lactates / Q000378:metabolism; D008659:Metabolic Diseases / Q000503:physiopathology*; D009369:Neoplasms / Q000150:complications / Q000378:metabolism*; D011488:Protein Deficiency / Q000150:complications; D011766:Pyruvate Carboxylase / Q000378:metabolism; D051381:Rats; D013379:Substrate Specificity
D000596:Amino Acids; D007773:Lactates; D000105:Acetyl Coenzyme A; D011766:Pyruvate Carboxylase; D005947:Glucose