Effect of Age and Dietary Fat Level on Fatty Acid Oxidation in the Neonatal Pig

Abstract

A total of 35 pigs were obtained by cesarean section, placed in individual sterile isolators, and randomly allotted to treatment groups. Thirty pigs received purified, isoenergetic liquid diets containing 2 or 32% butterfat (dry matter basis) and were killed at 1, 7, or 21 days of age. Five pigs were killed at 2 hours post delivery and received no diet. Twenty-one-day old pigs showed a tendency for higher weight gain and feed consumption when consuming the 32% fat diet although the differences were not significant. The rate of oxidation of [U-14C]palmitate to CO2 and acid soluble products was measured in homogenates of liver, kidney, heart, and leg muscle (biceps femoris) from pigs 0, 1, 7, and 21 days of age. The relative rates of oxidation of [U-14C]myristate, [U-14C]palmitate, and [U-14C]stearate were measured in homogenates of liver from 7-day old pigs. Palmitate oxidation was stimulated by carnitine in all four tissues and the rate of carnitine-stimulated palmitate oxidation to acid soluble products in heart and to CO2 in liver was higher in tissues from pigs consuming the 32% fat diet. The rate of palmitate oxidation increased with age in liver, kidney and leg muscle tissues and was maximum at 21 days in kidney and leg muscle and at 7 days in liver. The rate of palmitate oxidation in heart tended to decrease with animal age. In homogenates of liver from 7-day old pigs, palmitate was oxidized at a faster rate than stearate or myristate. The activities of carnitine palmitoyltransferase (CPT) (EC 2.3.1a) and succinate dehydrogenase (EC 1.3.99.1) in mitochondria isolated from liver, kidney, heart, and leg muscle did not vary considerably with age although CPT activity tended to be higher in those tissues from pigs consuming the high fat diet. Changes in the rate of palmitate oxidation with age tended to parallel changes in the level of mitochondrial protein per g of wet tissue and suggested an increased ability to utilize fat as an energy substrate during early development of the neonatal pig.

Hepatic ketogenesis in newborn pigs is limited by low mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase activity

“…It is noteworthy that the limitation of fatty acid oxidation was only restricted to the liver of newborn pigs, because fatty acid oxidation develops normally after birth in extra-hepatic tissues (Bieber et al, 1973;Wolfe et al, 1978;Ascuitto et al, 1989;Werner et al, 1989).…”

Fatty acid oxidation and ketogenesis during development

“…Similarly, compared to adults, the rate of palmitate oxidation is reduced in skeletal muscle homogenates (Glatz and Veerkamp, 1982 ;Carroll et al, 1983 ;Wolfe, Maxwell and Nelson, 1978 ;Mac Larty et al, 1984) and in kidney slices (Wolfe, Maxwell and Nelson, 1978 ;Freund, Sedraoui and Geloso, 1984), lung (Warshaw, Terry and Ranis, 1980) and small intestine (Warshaw, 1974) of fetal rats and pigs. As the rate of oxidation of octanoate, octanoylcarnitine or palmitoylcarnitine is similar in the heart of fetal, newborn and adult pigs and calves (Werner et al, 1983a, b ;Warshaw and Terry, 1970), it has been suggested that the reduced capacity of the fetal tissues to oxidize long-chain fatty acids could result from the low activity of carnitine acyltransferase I (Warshaw, 1972 ;Carroll et al, 1983 ;Delaval et al, 1984).…”

“…As newborn rats have a low ability to synthesize carnitine during the first postnatal week (Hahn, 1981) ln vitro studies using tissue homogenates (Warshaw, 1972 ;Glatz and Veerkamp, 1982 ;Wolfe, Maxwell and Nelson, 1978), isolated mitochondria (Warshaw and Terry, 1970 ;Werner et al, 1982) or isolated perfused organ (Werner et al, 1983b) have shown that the heart of fetal rats, rabbits, pigs and calves has a very low capacity for long-chain fatty acid oxidation, even in the presence of carnitine. Similarly, compared to adults, the rate of palmitate oxidation is reduced in skeletal muscle homogenates (Glatz and Veerkamp, 1982 ;Carroll et al, 1983 ;Wolfe, Maxwell and Nelson, 1978 ;Mac Larty et al, 1984) and in kidney slices (Wolfe, Maxwell and Nelson, 1978 ;Freund, Sedraoui and Geloso, 1984), lung (Warshaw, Terry and Ranis, 1980) and small intestine (Warshaw, 1974) of fetal rats and pigs.…”

“…The capacity of heart (Wittels and Bressler, 1965 ;Warshaw and Terry, 1970 ;Warshaw, 1972 ;Mersmann and Phinney, 1973 ;Aprille, 1976 ;Wolfe, Maxwell and Nelson, 1978 ;Werner et al, 1982Werner et al, , 1983a, skeletal muscle (Wolfe, Maxwell and Nelson, 1978 ;Glatz and Veerkamp, 1982 ;Carroll et al, 1983) and kidney (Wolfe, Maxwell and Nelson, 1978 ;Freund, Sedraoui and Geloso, 1984) to oxidize NEFA increases shortly after birth in rats, rabbits, pigs and calves. In contrast, it has been reported that substantial fatty acid oxidation occurs only 2 weeks after birth in dog heart (Breuer et al, 1968).…”

“…In contrast, it has been reported that substantial fatty acid oxidation occurs only 2 weeks after birth in dog heart (Breuer et al, 1968). Rosenthal and Warshaw (1977) (Aprille, 1976 ;Wolfe, Maxwell and Nelson, 1978).…”