Gluconeogenesis in tumor-influenced hepatocytes.
The growth of a tumor leads to alterations in host carbohydrate metabolism. In this study we examined gluconeogenic capacity and amino acid transport in tumor-influenced and control rat hepatocytes. Serum glucose level decreased with increasing tumor burden and a significant correlation (r = -0.80) was observed. Hepatic glycogen content was similar in both groups after an overnight fast. Endogenous glucose production was 27% higher in tumor-influenced hepatocytes. The presence of 10mM of alanine led to 72% stimulation of gluconeogenesis in tumor-influenced hepatocytes as compared to 48% stimulation in control hepatocytes. The same trends were present when lactate was used as a substrate. Alanine transport into the cells was increased in tumor-influenced hepatocytes by 55% +/- 5% at a physiologic level of substrate. In conclusion, gluconeogenesis from alanine and lactate is significantly increased in tumor-influenced hepatocytes despite decreased serum glucose levels. This is associated with increased gluconeogenic capacity and accelerated alanine transport.
D000409:Alanine / Q000378:metabolism; D000818:Animals; D001692:Biological Transport; D001786:Blood Glucose / Q000378:metabolism; D005943:Gluconeogenesis; D066298:In Vitro Techniques; D007773:Lactates / Q000502:physiology; D019344:Lactic Acid; D008099:Liver / Q000378:metabolism*; D008112:Liver Glycogen / Q000378:metabolism; D008297:Male; D051381:Rats; D011916:Rats, Inbred F344; D012513:Sarcoma, Experimental / Q000378:metabolism*
D001786:Blood Glucose; D007773:Lactates; D008112:Liver Glycogen; D019344:Lactic Acid; D000409:Alanine