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Carnitine Palmitoyltransferase Modulation of Hepatic Fatty Acid Metabolism and Radio-HPLC Evidence for Low Ketogenesis in Neonatal Pigs^1,2,3,

Jack Odle^*,,4, Xi Lin, Theo A. T. G. van Kempen^*,5, James K. Drackley^*,, and Sean H. Adams^*,6

^* Division of Nutritional Sciences Department of Animal Sciences, University of Illinois, Urbana, IL 61801

A neonatal piglet model was used to study hepatic fatty acid metabolism during the early postnatal period. Hepatocytes were isolated from pigs at birth or after 24 h, in fed or unfed states (n = 4 pigs/group). Cells were incubated with 1 mmol/L [1-¹⁴C]-octanoate (C8) or -palmitate (C16) in the presence or absence of 1 mmol/L L-carnitine, carnitine plus tetra-decylglycidic acid (TDGA; 10 µmol/L) or carnitine plus glucagon (0.5 µg/L). Accumulation of radiolabel [nmol/(h · 10⁶ cells)] in CO₂ and acid-soluble products (ASP) was higher (3.5- and 4.5-fold, respectively) from C8 than from C16 (P < 0.0001). Glucagon, carnitine and TDGA had no effect on the oxidation of C8 (P > 0.1). Carnitine addition tended to increase C16 flux to ASP [from 5.3 to 7.6 nmol/(h · 10⁶ cells); P < 0.1], whereas carnitine plus TDGA decreased flux (from 7.6 to 2.1; P < 0.001). Esterified products accounted for 70% of metabolized label in control C16 incubations; this was reduced to 62% by carnitine (P < 0.05) and increased to 80% by the addition of carnitine plus TDGA (P < 0.0001). The 1-¹⁴C flux to CO₂ in cells from 24-h-old unfed piglets was 47% lower than from fed pigs (P < 0.01) but 28% higher than in pigs at birth. Radiolabel contained in ASP and total metabolized label were 48% lower from unfed pigs compared with the piglets at birth and 24-h-old fed pigs (P < 0.01) and were paralleled by changes in oxygen consumption. Radio-HPLC analysis of ASP revealed minimal radiolabel accumulation in ketone bodies. Up to 40% of radioactivity in ASP was presumptively identified as acetate. These data illustrate that hepatic C16 metabolism in piglets can be altered by changes in the activity of carnitine palmitoyltransferase I during the neonatal period and that ketone bodies do not represent a major route of hepatic fatty acid carbon flux.

KEY WORDS: • swine • neonate • fatty acid metabolism • hepatocyte • ketogenesis

¹ Presented in abstract form at Experimental Biology 92, Anaheim, CA [Lin, X., Odle, J., van Kempen, T. & Drackley, J. (1992) The role of carnitine acyltransferase (CAT) in control of hepatic lipid metabolism in developing small-for-gestational-age piglets. FASEB J. 6: A1383 (abs.)].

² Supported by the Cooperative State Research Service, United States Department of Agriculture Grant #92-37203-7993 (project 35-0525), an International Life Sciences Institute Nutrition Foundation Future Leader Award, and the University of Illinois Agricultural Experiment Station (project #35-379).

³ The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

⁴ To whom correspondence and reprint requests should be addressed. Current address: Department of Animal Science, North Carolina State University, Raleigh, NC 27695-7621.

⁵ Current address: American Cyanamid, Princeton, NJ 08543.

⁶ Current address: Unit of Biochemistry, University of Barcelona, Barcelona, Spain 08028.

Manuscript received 9 December 1994. Revision accepted 5 April 1995.

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