Oxidation of Fatty Acids by Mitochondria Obtained from Newborn Subcutaneous (White) Adipose Tissue

Abstract

Oxidation of fatty acids was found to be both carnitine-dependent and carnitine-independent in mitochondria obtained from human newborn subcutaneous fat. A higher affinity of microsomes than that of mitochondria for free fatty acids was indirectly demonstrated by using microsomal fractions as substrate carriers. Oxygen consumption was detected in microsomal fractions and was associated with double bond formation. This may substantially contribute to the oxygen consumption of the developing adipocyte. The mechanisms involved in fatty acid oxidation in mitochondria of developing white adipocyte of the human newborn are similar to those described for mammalian brown fat.

Effect of Carnitine on Lipolysis in Subcutaneous Adipose Tissue of Newborns

“…We have previously found a similar effect in mitochondria of newborn subcutaneous white adipose tissue [16]. The scheme in figure 5 postulates a mechanism explaining the role of carnitine in the activation of lipolysis.…”

“…If such uncoupled mitochondria from brown adipose tissue are incubated in the presence of ATP and carnitine, respiration characteristic of oxidative phosphorylation (i.e. respiration dependent on phosphate acceptors -ADP or AMP) can be restored [9], This 'coupling' effect of carnitine has been detected also in the mitochondria of the sub cutaneous white adipose tissue of human newborns [16]. …”

Dietary Lipid and Postnatal Development. II. Palmityl Coenzyme A Oxidation in Heart and Liver

“…liver glycogen stores are present at birth, these are rapidly depleted (13,19). Once nursing commences, dietary lipid is a ready source of energy, but the capacity for fatty acid oxidation is deficient in MATERIALS the mammalian neonate (4,7,10,18,20); rapid maturation of the Crystalline BSA (fraction V), Pal-CoA, and ADP were all from enzymatic pathways for fatty acid oxidation (FAO) is suddenly Sigma Chemical Company.…”