Fatty Acid Oxidation by Developing Rat Kidney

Abstract

In view of the importance of free fatty acids (FFA) as substrates for the mature kidney, fatty acid oxidation by developing rat kidney has been investigated in vitro. Incubations of kidney slices from fetal stages (days 20 and 21 of gestation) and from days 1, 5, 10, 20, and 30 after birth have been carried out in Krebs-phosphate, pH 7.4, containing 0.5 or 1.5 mM/ U-¹⁴C-palmitate. Palmitate uptake and oxidation into CO₂ were measured after 90 min incubation. At 0.5 mM concentration of palmitate in the incubation medium, fetal kidney exhibited a low uptake and a very low oxidation of palmitate into CO₂. These two parameters increased only after birth and were maximum with slices from suckling rats between days 5 and 10 after birth. Palmitate oxidation increased only with postnatal days slices (maximum during the suckling period) and not with fetal slices. An increase in palmitate oxidation could be obtained with slices from kidneys of fetuses whose mothers had been starved 48h. These data suggest that the development of renal capacity for FFA oxidation during the perinatal period could be related to nutritional supply.

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).…”

“…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).…”

“…After weaning, this capacity remains elevated in heart (Warshaw, 1972 ;Glatz and Veerkamp, 1982 ;Werner et al, 1982), kidney (Novakova et al, 1980 ;Freund, Sedraoui and Geloso, 1984) and, to a lesser extent, in skeletal muscles (Glatz and Veerkamp, 1982 ;Carroll et al, 19831. This is not surprising since it is well known that NEFA are the preferred fuel of adult heart, kidney and resting muscles (see review by Owen and Reichard, 1974 (Callikan et al, 1979 ;Duée et al, 1983).…”

Changes in energy metabolism during the suckling and weaning period in the newborn

“…Lactate which comes from the incomplete oxidation of glucose in various tissues is a good gluconeogenic precursor in the newborn rat (Ferré et al, 1980 Jones, 1978aJones, , 1978b. At weaning lipoprotein lipase activity decreases in skeletal muscles and brown adipose tissue but remains elevated in the heart (Cryer and Jones, 1978aJones, , 1978b The capacity to oxidize long-chain fatty acids in extra-hepatic tissues is low in the fetal rat heart, skeletal muscle, kidney and small intestine but increases shortly after birth (Warshaw, 1972(Warshaw, , 1974Glatz and Veerkamp, 1982 ;Freund, Sedraoui and Geloso, 1984). It has been suggested that this is linked to a low activity during the fetal life of carnitine acyltransferase, the enzyme which catalyzes the entry of long-chain acylcoa inside the mitochondria, followed by its increase after birth, as well as to the increased concentration of its obligatory cofactor, carnitine, provided to the newborn via the milk (Robles-Valdes, McGarry and Foster, 1976 ;Borum, 1978 ;Hahn and Skala, 1972 ;Caroll et al, 1983).…”

“…It has been suggested that this is linked to a low activity during the fetal life of carnitine acyltransferase, the enzyme which catalyzes the entry of long-chain acylcoa inside the mitochondria, followed by its increase after birth, as well as to the increased concentration of its obligatory cofactor, carnitine, provided to the newborn via the milk (Robles-Valdes, McGarry and Foster, 1976 ;Borum, 1978 ;Hahn and Skala, 1972 ;Caroll et al, 1983). After weaning, the capacity to oxidize NEFA remains elevated in heart (Warshaw, 1972) ; kidney (Freund, Sedraoui and Geloso, 1984) and to a lesser extent in skeletal muscle (Glatz and Veerkamp, 1982).…”