Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.1.21 (CPT)
 4,580 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The enhancement of long-chain fatty acid oxidation and ketogenesis in the perfused rat liver, whether induced acutely by treatment of fed animals with anti-insulin serum or glucagon, or over the longer term by starvation or the induction of alloxan diabetes, was found to ba accompanied by a proportional elevation in the tissue carnitine content. Moreover, when added to the medium perfusing livers from fed rats, carnitine stimulated ketogenesis from oleic acid. The findings suggest that the increased fatty acid flux through the carnitine acyltransferase (carnitine palmitoyl-transferase; palmitoyl-CoA:L-carnitine O-palmitoyltransferase; EC 2.3.1.21) reaction brought about by glucagon excess, with or without insulin deficiency, is mediated, at least in part, by elevation in the liver carnitine concentration.
 ...
PMID:Role of carnitine in hepatic ketogenesis. 106 Jan 16

The effect of (+)-decanoylcarnitine, a potent inhibitor of long-chain acylcarnitine transferase, was tested for its ability to inhibit hepatic ketogenesis both in the isolated perfused liver and in vivo in severely ketotic alloxan diabetic rats. In vitro the inhibitor caused an almost complete block in ketone body production. In vivo (+)-decanoylcarnitine caused a rapid reversal of ketosis under conditions where large doses of insulin had little effect. A combination of the two agents produced an even more striking fall in plasma ketone levels.While (+)-decanoylcarnitine alone had no effect on plasma glucose levels it enhanced the hypoglycemic effect of insulin in anesthetized animals. Loss of this effect was noted in nonanesthetized animals, possibly as a result of increased muscle activity. Studies in the isolated perfused liver indicated that the blockade of fatty acid oxidation and ketogenesis produced by (+)-decanoylcarnitine was rapidly reversible upon removal of the inhibitor.
 ...
PMID:Acute reversal of experimental diabetic ketoacidosis in the rat with (+)-decanoylcarnitine. 463 91

Changes in fatty acid oxidation of peroxisomes in the liver of alloxan-diabetic rats were studied. After injection of alloxan (150 mg/kg, subcutaneously), the activity of peroxisomal cyanide-insensitive beta-oxidation increased more rapidly than that of carnitine palmitoyltransferase, which was the rate-limiting step of mitochondrial beta-oxidation, and reached 3 times the control level at 7 days after the treatment. The peroxisomal beta-oxidation activity was more potent toward medium chain acyl-CoAs (C=10 and 12), though it was extremely low for shorter chain lengths. The activity of carnitine acetyltransferase increased to 2.4 times the control level and the change appeared mainly in the peroxisomal fraction. On the other hand, the activity of palmitoyltransferase increased to twice the control level, distributed mostly in the mitochondrial fraction. The activity of carnitine acyltransferase increased mainly in the peroxisomal fraction, and was higher for shorter and medium chain acyl-CoAs. These results suggest that peroxisomal fatty acid oxidation and transport of acetyl-CoA and medium chain acyl-CoA as well as NADH product in peroxisomes may be rapidly enhanced in response to the demand of organs for the urgent supply of energy from fatty acids in the diabetic condition.
 ...
PMID:Changes in peroxisomal fatty acid oxidation in the diabetic rat liver. 733 4