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 frequently 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/M2) 1 to 5 years after liver transplantation and 8 healthy subjects (age 28.1+/-5.3 years, BMI 27.2+/-4.5 kg/M2). Subjects were studied while receiving an isoenergetic nutrition (based on 1.1 x their basal energy expenditure) as hourly oral liquid formula during 10 hours. Their hepatic DNL was measured by infusing 1-13C acetate and measuring tracer incorporation in VLDL-palmitate. Their glucose metabolism was assessed by means of 6,6-2H2 glucose and indirect calorimetry.


RESULTS
Two liver transplant recipients and 4 healthy subjects were obese, as defined by a BMI > 27 kg/M2. Fractional hepatic DNL was not different in the 2 groups of subjects: liver transplant recipients 3.1+/-1.7% vs 3.2+/-2.1% in healthy subjects. In both groups, DNL increased in proportion to BMI. When both groups were analyzed together, BMI was positively correlated with DNL (DNL = 0.28 x BMI - 4.28, r2 = .445, p < .05). Whole body glucose turnover was 15.0+/-4.4 micromol/kg per minute in liver transplant recipients and 15.8+/-4.1 micromol/kg per minute in healthy subjects (NS). Net carbohydrate oxidation tended to be lower in liver transplant recipients (8.1+/-2.6 micromol/kg per minute) than in healthy subjects (10.4+/-2.4 micromol/kg per minute; NS). Net nonoxidative glucose disposal (4.0+/-2.7 in liver transplant recipients vs 1.9+/-1.8 in healthy subjects, NS) and energy expenditure (0.065+/-0.01 vs 0.065+/-0.01 kJ/kg per minute) were similar in both groups.


CONCLUSIONS
These results indicate that fractional hepatic DNL is not altered by liver transplantation during near continuous nutrition. The disposal of orally administered carbohydrate is also essentially unchanged. This strongly argues against a role of hepatic DNL in the pathogenesis of obesity and dyslipidemia after liver transplantation.
Minehira
K
K
Institute of Physiology, Lausanne University School of Medicine, Switzerland.
Novel-Chaté
V
V
Schwarz
J M
JM
Gillet
M
M
Darioli
R
R
Chioléro
R
R
Tappy
L
L
D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D015992:Body Mass Index; D002153:Calorimetry, Indirect; D002247:Carbon Isotopes; D004040:Dietary Carbohydrates / Q000008:administration & dosage / Q000378:metabolism*; D005260:Female; D006801:Humans; D006949:Hyperlipidemias / Q000209:etiology; D008055:Lipids / Q000096:biosynthesis*; D008099:Liver / Q000378:metabolism*; D016031:Liver Transplantation / Q000009:adverse effects / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000209:etiology; D013379:Substrate Specificity
D001786:Blood Glucose; D002247:Carbon Isotopes; D004040:Dietary Carbohydrates; D008055:Lipids