Objective: To assess whether alterations in preoperative fatty acid ox
idation and gluconeogenesis induced by fasting will affect survival an
d liver regeneration following 90% hepatectomy in the rat. Design: In
a randomized, controlled trial, Wistar rats (N=157) were separated int
o 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 operati
on. These groups were further randomized to receive either 20% glucose
or tap water ad libitum postoperatively. Interventions: Ninety percen
t hepatectomy; 24-hour fast; 5% glucose feeding. Main Outcome Measures
: Survival, DNA synthesis in the hepatic remnant along with glucokinas
e activity (GKA) and glycogen content, serum ketone bodies (KB), free
fatty acid (FFA), glucose, and ad libitum glucose consumption (GC) wer
e 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 gluc
ose following hepatectomy (fed/ glucose), 95% vs 52% (P<.05) The faste
d/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<.
O5). Survival was poor in both groups when only tap water was offered
to the animals after hepatectomy (31% vs 12%). In the fasted/glucose g
roup, GC 1 hour after hepatectomy was greater than that for fed rats (
1.3 +/- .175 vs 0.73 +/- 0.176 g/h, P<.05), yet GKA was suppressed (3.
41 +/- 0.42 vs 8.05 +/- 2.77 nmol/min per milligrams of protein, P<.05
). Fasting before hepatectomy and consuming glucose after causes eleva
tions in both FFA (1.26 +/- 0.19 vs 0.82 +/- 0.13 mol/mL, P<.05) and K
B (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 a
t 8 hours after hepatectomy in the fed/ glucose group. Conclusions: Fa
sting before hepatectomy shifts energy utilization to fat oxidation an
d gluconeogenesis, which appears to ameliorate liver failure after hep
atectomy in this severe model of hepatic resection.