Developmental changes in carnitine palmitoyltransferases I and II gene expression in intestine and liver of suckling rats

Abstract

Carnitine palmitoyltransferase (CPT) I is expressed in the intestine of suckling rats; its mRNA increases very rapidly after birth, remains on a plateau until day 18 and decreases until weaning, when basal (adult) values are reached, which remain unchanged thereafter. CPT II mRNA values do not show any appreciable change in this period. CPT I and CPT II are expressed mainly in mucosa and, to a lesser extent, in the muscular part of the intestine. Intestinal expression of CPT I is maximal in duodenum and jejunum, whereas CPT II is expressed in a similar pattern throughout the whole intestine. Dam's milk may influence the intestinal expression of CPT I, since mRNA levels at birth are low but increase after the first lactation. Moreover, rats weaned at either day 18 or 21 decrease their mRNA levels. Apparently, CPT II gene expression is not influenced by the mother's milk. CPT I and CPT II are also expressed in the liver of suckling rats. Hepatic CPT I is maximal at day 3, and levels of CPT II mRNA do not change, in a similar fashion to that in intestine. The profile of expression of CPT I in liver and intestine strongly resembles that previously reported for mitochondrial 3-hydroxy-3-methyl-glutaryl-CoA synthase.

Gene expression of mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase in a poorly ketogenic mammal: effect of starvation during the neonatal period of the piglet

“…Ketogenesis is also associated with increased substrate availability and changes in the activities of enzymes central to β-oxidation. Perinatal and dietary responses of rat hepatic mitochondrial HMG-CoA synthase coincide with changes in the expression and activity of liver carnitine palmitoyl transferase I (CPT-I) [6,[12][13][14][15], which suggests common regulatory mechanisms for these genes.…”

“…The increased ketogenesis in newborn rats is due to transcriptional and post-transcriptional factors, including the induction of the expression of mitochondrial HMG-CoA synthase and CPT-I gene [9,10,14,15] and the depressed inhibition of these enzymes by succinyl-CoA and malonyl-CoA respectively [4].…”

Isolation of pig mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase gene promoter: characterization of a peroxisome proliferator-responsive element

“…During the neonatal period, emerging liver fatty acid metabolism involves the rise of mRNA levels for at least two main controlling genes (i.e., carnitine palmitoyltransferase I and mitochondrial HMG-CoA synthase) [9,10,40,41]. Such changes of gene expression have been correlated with nutritional and hormonal The transcription start site, indicated by arrows, was determined by 5-RACE for the human [44] and pig (the present study) genes, and by primer extension and S1 experiments for the rat [52] gene.…”

Inhibition of carnitine palmitoyltransferase in the rat small intestine reduces export of triacylglycerol into the lymph

“…The net effect of the CPT enzyme system, linked to the carnitine-acylcarnitine translocase, is net movement of acyl-groups across the inner mitochondrial membrane. This mitochondrial CPT system exists in all mammalian cells, including small intestine (14). Although two isoforms of CPT-I, known as CPT-I ␣ and CPT-I ␤ , have been cloned (15)(16)(17), only CPT-I ␣ is expressed in the liver and small intestine (14).…”

“…This mitochondrial CPT system exists in all mammalian cells, including small intestine (14). Although two isoforms of CPT-I, known as CPT-I ␣ and CPT-I ␤ , have been cloned (15)(16)(17), only CPT-I ␣ is expressed in the liver and small intestine (14). Mitochondrial CPT-I is inhibited by malonyl-CoA, which is a precursor for FA synthesis (13), and the sensitivity of CPT-I ␣ to malonyl-CoA inhibition is increased by insulin and decreased by fasting (18)(19)(20).…”