Hepatic de novo lipogenesis after liver transplantation

Background: The liver can synthesize fatty acids from carbohydrate (de novo lipogenesis [DNL]).We hypothesized that stimulation of this process may be involved in the development of obesity and dyslipidemia, 2 conditions freq uently encountered after liver transplantation. Methods: Hepatic fractional DNL and glucose metabolism were measured in 2 groups of 5 patients (age 36 .8 +/- [SD] 14.9 years, BMI 26.3 +/- 5.3 kg/m(2)) 1 to 5 years after liver transplantation and 8 healthy subjects (age 28.1 +/- 5.3 years, BMI 27.2 +/ - 4.5 kg/m(2)). Subjects were studied while receiving an isoenergetic nutri tion (based on 1.1 X their basal energy expenditure) as hourly oral liquid formula during 10 hours. Their hepatic DNL was measured by infusing 1-C-13 acetate and measuring tracer incorporation in VLDL-palmitate. Their glucose metabolism was assessed by means of 6,6-H-2(2) glucose and indirect calori metry. Results: Two liver transplant recipients and 4 healthy subjects were obese, as defined by a BMI > 27 kg/m(2). Fractional hepatic DNL was not di fferent in the 2 groups of subjects: liver transplant recipients 3.1 +/- 1. 7% us 3.2 +/- 2.1% in healthy subjects. In both groups, DNL increased in pr oportion to BMI. When both groups were analyzed together, BMI was positivel y correlated with DNL (DNL = 0.28 X BMI - 4.28, r(2) = .445, p < .05). Whol e body glucose turnover was 15.0 +/- 4.4 mu mol/kg per minute in liver tran splant recipients and 15.8 +/- 4.1 mu mol/kg per minute in healthy subjects (NS). Net carbohydrate oxidation tended to be lower in liver transplant re cipients (8.1 +/- 2.6 mu mol/kg per minute) than in healthy subjects (10.4 - +/- 2.4 mu mol/kg per minute; NS). Net nonoxidative glucose disposal (4.0 - +/- 2.7 in liver transplant recipients us 1.9 +/- 1.8 in healthy subject s, NS) and energy expenditure (0.065 +/- 0.01 us 0.065 0.01 kJ/kg per minut e) were similar in both groups. Conclusions: These results indicate that fr actional hepatic DNL is. not altered by liver transplantation during near c ontinuous nutrition. The disposal of orally administered carbohydrate is al so essentially unchanged. This strongly argues against a role of hepatic DN L in the pathogenesis of obesity and dyslipidemia after liver transplantati on.