Glucose overload and hepatic energy metabolism after resection of the cirrhotic liver in rats.
The effect of glucose hyperalimentation on energy metabolism in the cirrhotic rat liver after 70% hepatectomy was studied. After resection, rats received either 30 kcal/kg per day (group I) or 200 kcal/kg per day (group II) of glucose for 48 h. In both groups, hepatic mitochondrial ATP synthesis was accelerated when palmitic acid was used as substrate and suppressed when pyruvate was used. This suggests that the energy substrate of the remnant liver was principally fatty acids rather than glucose. Hepatic energy charge was within normal limits in group I, but decreased significantly in group II after hepatectomy. An abundance of glucose in the early postoperative period, therefore, caused a hepatic energy derangement by suppressing fatty acids utilization; this suppression was corroborated by the findings of lower immunoreactive glucagon and non-esterified fatty-acid concentrations in group II. To determine optimal glucose administration, the predicted value of glucose disposal rate (GDR) was calculated after an intravenous glucose tolerance test. GDR decreased significantly after hepatectomy and did not increase appreciably even with a large dose of insulin administration. These results suggest that glucose administration should be tailored to the GDR values after resection of the cirrhotic liver.
Ouchi
K
K
Department of Surgery, Tohoku University School of Medicine, Sendai, Japan.
Sakai
K
K
Sato
R
R
Mikuni
J
J
Matsuno
S
S
D000255:Adenosine Triphosphate / Q000096:biosynthesis; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D004040:Dietary Carbohydrates / Q000008:administration & dosage / Q000494:pharmacology; D002149:Energy Intake; D004734:Energy Metabolism / Q000187:drug effects*; D005227:Fatty Acids / Q000378:metabolism; D005934:Glucagon / Q000378:metabolism; D005947:Glucose / Q000008:administration & dosage / Q000378:metabolism / Q000494:pharmacology*; D006498:Hepatectomy; D006943:Hyperglycemia / Q000139:chemically induced / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008106:Liver Cirrhosis, Experimental / Q000378:metabolism / Q000601:surgery*; D008297:Male; D008930:Mitochondria, Liver / Q000187:drug effects / Q000378:metabolism; D019308:Palmitic Acid; D010169:Palmitic Acids / Q000494:pharmacology; D011184:Postoperative Period; D011773:Pyruvates / Q000378:metabolism; D019289:Pyruvic Acid; D051381:Rats; D011919:Rats, Inbred Strains
D001786:Blood Glucose; D004040:Dietary Carbohydrates; D005227:Fatty Acids; D010169:Palmitic Acids; D011773:Pyruvates; D019308:Palmitic Acid; D019289:Pyruvic Acid; D000255:Adenosine Triphosphate; D005934:Glucagon; D005947:Glucose