Preoperative fasting improves survival after 90% hepatectomy.
OBJECTIVE
To assess whether alterations in preoperative fatty acid oxidation and gluconeogenesis induced by fasting will affect survival and liver regeneration following 90% hepatectomy in the rat.


METHODS
In a randomized, controlled trial, Wistar rats (N = 157) were separated into two groups. Rats in the first group fasted for 24 hours. Rats in the second group were allowed to eat ad libitum until the time of operation. These groups were further randomized to receive either 20% glucose or tap water ad libitum postoperatively.


METHODS
Ninety percent hepatectomy; 24-hour fast; 5% glucose feeding.


METHODS
Survival, DNA synthesis in the hepatic remnant along with glucokinase activity (GKA) and glycogen content, serum ketone bodies (KB), free fatty acid (FFA), glucose, and ad libitum glucose consumption (GC) were serially quantified.


RESULTS
Fasting rats that were offered glucose (fasted/glucose) after hepatectomy demonstrated better survival at 48 hours than the rats that were fed before the procedure and given glucose following hepatectomy (fed/glucose), 95% vs 52% (P < .05). The fasted/glucose group also had a greater peak rate of DNA synthesis (550 +/- 110 vs 275 +/- 40 disintegrations per minute per 0.001 mg of DNA, P < .05). Survival was poor in both groups when only tap water was offered to the animals after hepatectomy (31% vs 12%). In the fasted/glucose group, GC 1 hour after hepatectomy was greater than that for fed rats (1.3 +/- 0.175 vs 0.73 +/- 0.176 g/h, P < .05), yet GKA was suppressed (3.4 +/- 0.42 vs 8.05 +/- 2.77 nmol/min per milligrams of protein, P < .05). Fasting before hepatectomy and consuming glucose after causes elevations in both FFA (1.26 +/- 0.19 vs 0.82 +/- 0.13 mol/mL., P < .05) and KB (18.96 +/- 2.82 vs 11.4 +/- 3.94 mmol/mL, P < .05). Normal glucose was maintained in the fasted/glucose group, but fell to 63 +/- 14 mg/dL at 8 hours after hepatectomy in the fed/glucose group.


CONCLUSIONS
Fasting before hepatectomy shifts energy utilization to fat oxidation and gluconeogenesis, which appears to ameliorate liver failure after hepatectomy in this severe model of hepatic resection.
Sarac
T P
TP
Department of Surgery, University of Rochester Medical Center, NY.
Sax
H C
HC
Doerr
R
R
Yuksel
U
U
Pulli
R
R
Caruana
J
J
D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D003131:Combined Modality Therapy; D004247:DNA / Q000096:biosynthesis; D005215:Fasting; D005227:Fatty Acids / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005941:Glucokinase / Q000032:analysis; D005943:Gluconeogenesis; D005947:Glucose / Q000627:therapeutic use; D006003:Glycogen / Q000032:analysis; D006498:Hepatectomy / Q000401:mortality*; D007657:Ketone Bodies / Q000097:blood; D015993:Life Tables; D017093:Liver Failure / Q000378:metabolism / Q000401:mortality* / Q000473:pathology / Q000628:therapy*; D008115:Liver Regeneration; D010084:Oxidation-Reduction; D011182:Postoperative Care; D011300:Preoperative Care; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D015996:Survival Rate; D013997:Time Factors
D001786:Blood Glucose; D005227:Fatty Acids; D005230:Fatty Acids, Nonesterified; D007657:Ketone Bodies; D006003:Glycogen; D004247:DNA; D005941:Glucokinase; D005947:Glucose