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PubMed2005

Carnitine treatment inhibits increases in cerebral carnitine esters and glutamate detected by mass spectrometry after hypoxia-ischemia in newborn rats.

BACKGROUND AND PURPOSE: Cerebral ischemic insults disrupt normal respiratory activity in mitochondria. Carnitine plays an essential role in mitochondrial metabolism and in modulating excess acyl-coenzyme A (acyl-CoA) levels. The effects of cerebral ischemia on carnitine metabolism are not well understood, although the newborn may be particularly vulnerable to carnitine deficiency. We used a newborn rat model of hypoxia-ischemia (HI) to test the hypothesis that HI alters acyl-CoA:CoA homeostasis and that this effect can be prevented by treatment with carnitine. METHODS: A total of 120 postnatal day 7 rats were subjected to 70 minutes of HI after treatment with 16 mmol/kg intraperitoneal l-carnitine or diluent. Carnitine, acylcarnitines, and excitatory amino acids were measured by mass spectrometry, and carnitine acetyl transferase activity, superoxide, and levels of the mitochondrial phospholipid cardiolipin (CL) were measured at 2- and 24-hour recovery. RESULTS: HI and hypoxia were associated with a significant increase in the ratio of acyl-CoA:CoA, which was prevented by treatment with carnitine. Carnitine treatment also prevented increases in glutamate, glycine, superoxide, and decrease of CL. CONCLUSIONS: Carnitine metabolic pathways are compromised in HI and hypoxia. The protective effect of carnitine treatment on HI injury may be attributable to maintaining mitochondrial function.

Animals↗
PubMed1993

Carnitine acyltransferase enzymic catalysis requires a positive charge on the carnitine cofactor.

3-Hydroxy-5,5-dimethylhexanoic acid (HDH) is an analogue of carnitine which differs only in the substitution of a quaternary carbon atom for the quaternary ammonium nitrogen. Thus HDH is isosteric with carnitine but lacks the quaternary ammonium positive charge. Racemic HDH, each of its enantiomers, and the O-acetyl derivative (Ac-HDH) were evaluated as alternate substrates and inhibitors for several carnitine acyltransferases. HDH and Ac-HDH are not substrates for carnitine acetyltransferase (CAT) at concentrations up to 10 mM, suggesting that the positive quaternary ammonium charge on carnitine is essential for CAT catalysis. However, HDH competitively inhibits CAT (Ki = 8.3 mM), carnitine palmitoyltransferase-I (CPT-I) (Ki = 3.6 mM), and CPT-II (Ki = 2.8 mM). Ac-HDH is also a competitive inhibitor of CAT when assayed in the reverse direction (Ki = 4.1 mM). Similarly, R-(+)-HDH and S-(-)-HDH are not substrates for CAT, but they are stereoselective competitive inhibitors (Ki = 20.3 and 7.5 mM for the R and S enantiomers, respectively). Stereoselective inhibition by HDH is even more dramatic with CPT-I, since S-(-)-HDH inhibits CPT-I (Ki = 1.4 mM) but R-(+)-HDH has no effect in concentrations up to 5 mM. As with CAT, HDH is a stereoselective inhibitor of CPT-II, and the Ki values for S-(-)- and R-(+)-HDH are 2.2 and 6.7 mM, respectively. Since the observed Ki values are significantly larger than the Km for carnitine, the positive charge on carnitine must also be important, but not essential, for binding to the carnitine site on carnitine acyltransferases.

Animals↗
PubMed1991

Carnitine in muscle, serum, and urine of nonprofessional athletes: effects of physical exercise, training, and L-carnitine administration.

Efficient utilization of fatty acids to sustain prolonged physical efforts is thought to be dependent on the carnitine shuttle of muscle. A study has been carried out in 24 athletes (13 long-distance runners and 11 sprinters). These subjects received placebo or L-carnitine (1 g/orally b.i.d.) during a 6-month period of training. In endurance athletes, training induced lowering of total and free muscle carnitine. Increase of esterified muscle carnitine was also observed. Post-exertional overflow of acetylcarnitine and long-chain acylcarnitine, as well as reduction of the free fraction was also noticed in the blood. Fasting plasma carnitine levels, however, were not affected in carnitine-treated athletes at rest. These changes were likely related with the significantly increased urinary excretion of esterified and total carnitine which occurred after physical exercise. In the sprinters only, a decrease in free and total carnitine of muscle was detected after training. Both these potentially unfavorable effects were prevented by oral administration of L-carnitine. Our data suggest that training in endurance athletes, and to a lesser extent, in sprinters, is associated with a decrease in free and total carnitine of muscle, due to an increased overflow of short-chain carnitine esters in urine.

Adult↗
PubMed2006

Involvement of recognition and interaction of carnitine transporter in the decrease of L-carnitine concentration induced by pivalic acid and valproic acid.

PURPOSE: Prodrugs with pivalic acid and valproic acid decrease L-carnitine concentration in plasma and tissues by urinary excretion of acylcarnitine as pivaloylcarnitine (PC) and valproylcarnitine (VC), respectively. We investigated the role of the Na+/L-carnitine cotransporter in the porcine kidney epithelial cell line, LLC-PK1 for the decrease of L-carnitine concentration. METHODS: The uptake of L-[3H]carnitine, acetyl-L-[3H]carnitine (AC), L-[3H]PC and L-[3H]VC were investigated in LLC-PK1 cells seeded in a 6-well culture plate. RESULTS: L-Carnitine and AC uptake in LLC-PK1 cells exhibited Na+ dependency. The Km values for L-carnitine and AC uptake were 11.0 and 8.18 microM, respectively. These results indicated expression of Na+/ L-carnitine cotransporter in LLC-PK1 cells. PC and VC inhibited Na+/L-carnitine cotransporter in the competitive (Ki = 90.4 microM) and noncompetitive (Ki = 41.6 microM) manners, respectively. PC and VC uptake by Na+/L-carnitine cotransporter were not observed in LLC-PK1 cells. CONCLUSIONS: These data suggested that PC and VC formed in the body could not be reabsorbed in the kidney, resulting in the decrease of L-carnitine concentration. In addition, inhibition of L-carnitine reabsorption by VC with lower Ki value could induce the decrease of L-carnitine concentration. Collectively, the recognition and interaction of Na+/L-carnitine cotransporter are important factors for carnitine homeostasis.

Acetylcarnitine↗
PubMed1995

Effects of L-carnitine administration on left ventricular remodeling after acute anterior myocardial infarction: the L-Carnitine Ecocardiografia Digitalizzata Infarto Miocardico (CEDIM) Trial.

OBJECTIVES: This study was performed to evaluate the effects of L-carnitine administration on long-term left ventricular dilation in patients with acute anterior myocardial infarction. BACKGROUND: Carnitine is a physiologic compound that performs an essential role in myocardial energy production at the mitochondrial level. Myocardial carnitine deprivation occurs during ischemia, acute myocardial infarction and cardiac failure. Experimental studies have suggested that exogenous carnitine administration during these events has a beneficial effect on function. METHODS: The L-Carnitine Ecocardiografia Digitalizzata Infarto Miocardico (CEDIM) trial was a randomized, double-blind, placebo-controlled, multicenter trial in which 472 patients with a first acute myocardial infarction and high quality two-dimensional echocardiograms received either placebo (239 patients) or L-carnitine (233 patients) within 24 h of onset of chest pain. Placebo or L-carnitine was given at a dose of 9 g/day intravenously for the first 5 days and then 6 g/day orally for the next 12 months. Left ventricular volumes and ejection fraction were evaluated on admission, at discharge from hospital and at 3, 6 and 12 months after acute myocardial infarction. RESULTS: A significant attenuation of left ventricular dilation in the first year after acute myocardial infarction was observed in patients treated with L-carnitine compared with those receiving placebo. The percent increase in both end-diastolic and end-systolic volumes from admission to 3-, 6- and 12-month evaluation was significantly reduced in the L-carnitine group. No significant differences were observed in left ventricular ejection fraction changes over time in the two groups. Although not designed to demonstrate differences in clinical end points, the combined incidence of death and congestive heart failure after discharge was 14 (6%) in the L-carnitine treatment group versus 23 (9.6%) in the placebo group (p = NS). Incidence of ischemic events during follow-up was similar in the two groups of patients. CONCLUSIONS: L-Carnitine treatment initiated early after acute myocardial infarction and continued for 12 months can attenuate left ventricular dilation during the first year after an acute myocardial infarction, resulting in smaller left ventricular volumes at 3, 6 and 12 months after the emergent event.

Adult↗
PubMed2006

Prolonged effect of single carnitine administration on fasted carnitine-deficient JVS mice regarding their locomotor activity and energy expenditure.

Carnitine is an essential cofactor for the oxidation of fatty acid in the mitochondria and an efficient therapeutics for primary carnitine deficiency. We herein analyzed the prolonged effects of carnitine on the reduced locomotor activity and energy metabolism of fasted carnitine-deficient juvenile visceral steatosis (jvs(-/-)) mice. We found that a single carnitine administration to 24-h fasted jvs(-/-) mice in the morning increased both the locomotor activity and oxygen consumption at night not only on the same day, but also on the next day, when the carnitine levels in the blood and tissues were already as low as at the original carnitine-deficient state. We also found that fat utilization for energy production significantly increased under fasting even in jvs(-/-) mice and was stimulated in the carnitine-administrated fasted jvs(-/-) mice at night, in comparison to that observed in the saline-administered jvs(-/-) mice, at least for 2 days even under the low plasma and tissue carnitine levels. These results suggest that the low tissue carnitine levels are therefore not the sole rate-limiting factor of general fatty acid oxidation in carnitine-deficient jvs(-/-) mice.

Animals↗
PubMed2005

Carnitine depletion in rat pups from mothers given mildronate: a model of carnitine deficiency in late fetal and neonatal life.

Mildronate (3-(2,2,2,-trimethylhydrazinium)propionate), is a butyrobetaine analogue that is known to inhibit gamma-butyrobetaine hydroxylase, the enzyme catalyzing the last step of carnitine biosynthesis. When administered to adult rats it determines a systemic carnitine deficiency and may therefore serve as an animal model for human carnitine depletion. The aim of this study was to evaluate the effect of mildronate administration to pregnant and lactating rats on tissue carnitine concentrations in 4- and 13-day-old rat pups. At 14 days of gestation female rats began to receive mildronate in the diet (200 mg/kg/d) and this continued for entire lactation period. Mildronate treatment determined a large reduction of carnitine levels in the milk of lactating dams. Because organ carnitine concentrations in neonatal rats are directly related to dietary supply, pups from mildronate group had significantly depleted levels of total carnitine in serum, heart, liver, muscle, brain and pancreas relative to controls, at 4 and 13 days of age. Correspondingly, an increase in triglyceride levels was observed in liver, heart and muscle of mildronate pups. This is in agreement with a reduction of basal rate of oxidation of [U-(14)C]-palmitate to (14)CO(2) and (14)C-acid-soluble products observed in liver homogenates from carnitine-deficient pups. All functional and biochemical modifications were compatible with a carnitine deficiency status. In conclusion our results describe a model of carnitine depletion in pups, suitable for the investigation of carnitine deficiency in fetal-neonatal nutrition, without any concomitant mildronate-mediated metabolic alterations.

Animals↗
PubMed1989

Quantitation of urinary carnitine esters in a patient with medium-chain acyl-coenzyme A dehydrogenase deficiency: effect of metabolic state and L-carnitine therapy.

Urinary carnitine esters were quantitated in an infant with medium-chain acylcoenzyme A dehydrogenase deficiency by means of a highly sensitive and specific radioisotopic exchange high-pressure liquid chromatography method. During fasting, the excretion of free carnitine and of acetylcarnitine, octanoylcarnitine, and hexanoylcarnitine was increased. The fractional tubular reabsorption of free carnitine was decreased, suggesting a renal leak of free carnitine. In the symptom-free, fed state, only minor amounts of free carnitine and of short-chain acylcarnitine, octanoylcarnitine, and hexanoylcarnitine were present in urine, and carnitine loss occurred in the form of "other" carnitine esters not exceeding that of control subjects. During L-carnitine therapy, the excretion of free carnitine, short-chain acylcarnitine, octanoylcarnitine, and hexanoylcarnitine, and particularly of "other" carnitine esters, was increased, suggesting a possible detoxifying effect of administered carnitine that is not confined to the elimination of octanoic and hexanoic acids. The employed method detects very low urinary concentrations of octanoylcarnitine and hexanoylcarnitine (less than 1 mumol/L) characteristic of medium-chain acyl-coenzyme A dehydrogenase deficiency and may be useful in screening for this disease, which has been associated with sudden infant death.

Acetylcarnitine↗
PubMed1997

Purification and characterization of D(+)-carnitine dehydrogenase from Agrobacterium sp.--a new enzyme of carnitine metabolism.

D(+)-Carnitine dehydrogenase from Agrobacterium sp. catalyzes the oxidation of D(+)-carnitine to 3-dehydrocarnitine as initial step of D(+)-carnitine degradation. The NAD(+)-specific, cytosolic enzyme was purified 126-fold to apparent electrophoretic homogeneity by 4 chromatographic steps. The molecular mass of the native enzyme was estimated to be 88 kDa by size-exclusion chromatography. It seems to be composed of 3 identical subunits with a relative molecular mass of 28 kDa as found by sodium dodecyl sulfate polyacrylamide gel electrophoresis and laser-induced mass spectrometry. The isoelectric point was found to be 4.7-5.0. The optimum temperature is 37 degrees C and the optimum pH for the oxidation and the reduction reaction are 9.0-9.5 and 5.5-6.5, respectively. The purified enzyme was further characterized with respect to substrate specificity, kinetic parameters and amino terminal sequence. Analogues of D(+)-carnitine (L(-)-carnitine, crotonobetaine, gamma-butyrobetaine, carnitine amide, glycine betaine, choline) are competitive inhibitors of D(+)-carnitine oxidation. The equilibrium constant of the reaction of D(+)-carnitine dehydrogenase was determined to be 2.2 x 10(-12). The purified D(+)-carnitine dehydrogenase has similar kinetic properties to the L(-)-carnitine dehydrogenase from the same microorganism as well as to L(-)-carnitine dehydrogenases of other bacteria.

Alcohol Oxidoreductases↗
PubMed2003

L-carnitine transport in kidney of normotensive, Wistar-Kyoto rats: effect of chronic L-carnitine administration.

PURPOSE: To examine the effect of long-term administration of L-carnitine on L-carnitine transport in renal brush-border membrane vesicles (BBMVs) from normotensive, Wistar-Kyoto rats. METHODS: Rats (n = 20) were orally administered 0.2 g carnitine/kg body weight per day for a total period of 8 weeks. Kinetic parameters of L-carnitine uptake were calculated by non-linear regression, and the relative abundance of the carnitine transporter, OCTN2, was determined by Western blot analysis. RESULTS: Initial rates and maximal overshoot levels of Na+-dependent L-carnitine transport were significantly reduced in BBMVs from L-carnitine-treated rats compared with untreated animals. Similarly, the maximal transport rate (Vmax) of OCTN2 was lower in treated rats. However, no differences were observed in the Michaelis constant (Km) or the diffusion constant (Kd) between the two groups of animals. The amount of OCTN2 protein was also decreased in L-carnitine-fed rats, this reduction being similar to that of the Vmax. These results were accompanied by an increase in the serum levels and also in the renal excretion of both free and esterified carnitine in treated rats, indicating that the long-term administration of L-carnitine leads to increased renal carnitine clearance. CONCLUSION: These findings suggest a downregulation of OCTN2 at the renal level, in the presence of high levels of carnitine.

Animals↗
PubMed1994

Effect of intravenous L-carnitine on carnitine homeostasis and fuel metabolism during exercise in humans.

This study was undertaken to challenge the hypothesis that short-term administration of carnitine during exercise can modify skeletal muscle carnitine homeostasis and fuel metabolism in normal humans. With a randomized, blinded, crossover design, subjects received carnitine or placebo at the start of a bicycle ergometer exercise session. During the 2 hours after intravenous administration of 185 mumol/kg carnitine, carnitine kinetics could be described with a central compartment volume of distribution of 200 ml/kg, a total clearance from this compartment of 1.9 ml/min/kg, and a renal clearance of 1.3 ml/min/kg. Carnitine administration had no effect on muscle total carnitine content or the workload-dependent accumulation of acylcarnitines in skeletal muscle. Carnitine had no effect on the respiratory exchange ratio, muscle lactate accumulation, plasma lactate concentration, muscle glycogen utilization, or plasma beta-hydroxybutyrate concentration during exercise. Thus the skeletal muscle carnitine pool is segregated from dramatic changes in the plasma carnitine pool, and short-term administration of carnitine has no significant effect on fuel metabolism during exercise in humans.

Adult↗
PubMed1970

Specific alkylation of a histidine residue in carnitine acetyltransferase by bromoacetyl-L-carnitine.

Incubation of carnitine acetyltransferase with low concentrations of bromoacetyl-l-carnitine causes a rapid and irreversible loss of enzyme activity; one mol of inhibitor can inactivate one mol of enzyme. Bromoacetyl-d-carnitine, iodoacetate or iodoacetamide are ineffective. l-Carnitine protects the transferase from bromoacetyl-l-carnitine. Investigation shows that the enzyme first reversibly binds bromoacetyl-l-carnitine with an affinity similar to that shown for the normal substrate acetyl-l-carnitine; this binding is followed by an alkylation reaction, forming the carnitine ester of a monocarboxymethyl-protein, which is catalytically inactive. The carnitine is released at an appreciable rate by spontaneous hydrolysis, and the resulting carboxymethyl-enzyme is also inactive. Total acid hydrolysis of enzyme after treatment with 2-[(14)C]bromoacetyl-l-carnitine yields N-3-carboxy[(14)C]methylhistidine as the only labelled amino acid. These findings, taken in conjunction with previous work, suggest that the single active centre of carnitine acetyltransferase contains a histidine residue.

Acetates↗
PubMed2005

Pregnancy increases urinary loss of carnitine and reduces plasma carnitine in Korean women.

This study compared plasma and urinary carnitine concentrations in pregnant and non-pregnant Korean women. The subjects were fifty pregnant women and thirty non-pregnant women aged 24-28 years. During the first trimester, dietary carnitine intakes in the pregnant women were much lower than in non-pregnant women (70.00 (SD 29.22) micromol/d), but over the course of pregnancy carnitine intake increased from 44.64 (SD 24.84) micromol/d during the first trimester to 96.11 (SD 36.56) micromol/d during the third trimester. Pregnant women had a significantly lower plasma carnitine concentration than non-pregnant women. Plasma concentrations of non-esterified carnitine, acid-soluble acylcarnitine and total carnitine were significantly lower during the second and third trimesters than the first. Plasma acid-insoluble acylcarnitine levels, which tended to be higher in the non-pregnant women compared with the pregnant women, increased significantly as gestation proceeded. The urinary excretion of non-esterified carnitine, acid-soluble acylcarnitine and total carnitine was significantly higher in the pregnant women during the first and second trimesters than in non-pregnant women and decreased significantly as gestation proceeded. We found that there was a significant decrease in plasma carnitine level even though dietary carnitine intake increased as gestation proceeded. The low urinary excretion of carnitine in late pregnancy may be caused by an increased demand during pregnancy.

Adult↗
PubMed2005

Gestational diabetes exhibits lack of carnitine deficiency despite relatively low carnitine levels and alterations in ketogenesis.

OBJECTIVE: Previous studies have underlined the importance of the carnitine shuttle system and its dysfunction both in normal pregnancy and in type 1 and 2 diabetes. The objective of this paper was to delineate more systematically the role of the carnitine shuttle system in normal pregnancy and in gestational diabetes. METHODS: A total of 119 women matched for age comprised three groups: 40 normal adult non-pregnant women (NNP), 46 normal pregnant women with uncomplicated pregnancy (NP) and 33 women with gestational diabetes (GDM). The latter group was further subdivided into those being managed either by diet alone (25 women, GDM-D) or by insulin (8 women,GDM-I). The following biochemical parameters were assayed: fasting plasma total, free and acyl-carnitine, FFA and beta-OH-butyrate, together with several essential anthropometric parameters. RESULTS: Women with GDM, in contrast to the control groups, displayed the biochemical features characteristic of insulin resistance: higher body weight, higher BMI, higher skinfold and higher HbAlc levels. No differences on any parameters were found between the two GDM subgroups. Both NP and GDM groups had low levels of total carnitine compared to NNP control group, but surprisingly, the GDM group did not exhibit any further decrease of carnitine levels, as would have been expected by the combination of pregnancy and diabetes. Both groups, despite these low carnitine levels, had no clinical symptoms of carnitine deficiency. Furthermore, the GDM group displayed higher levels of FFA and beta-hydroxybutyrate, which were statistically significant compared to the other two control groups. CONCLUSIONS: The data corroborate the negative effect of normal gestation on the carnitine shuttle system, while they document for the first time that GDM does not further affect the efficiency of the carnitine system. The mild effect of GDMon carnitine status could be explained by the concurrent increased gluconeogenesis, a process which does not affect directly carnitine metabolism.

3-Hydroxybutyric Acid↗
PubMed1991

Dietary carnitine effects on carnitine concentrations in urine and milk in lactating women.

The effect of dietary carnitine on urinary excretion of free and total carnitine and on breast-milk secretion of the carnitine fractions in 15 control and 16 lactating women aged 21-40 y was measured. Free and total carnitine excretions, obtained from 24-h urine collections, correlated with carnitine consumed on the collection day (P less than 0.03, P less than 0.01, respectively) but not with the mean intake calculated from 3-d diet records. The immediate responses of the control and lactating groups were not significantly different. Urinary excretion of carnitine (n = 31) was 82 +/- 13 mumol/d for free excretion and 226 +/- 22 mumol/d for total excretion. Milk free, acid-soluble acyl-, acid-insoluble acyl-, or total carnitine did not correlate with dietary carnitine or with the duration of lactation (1-10 mo). Milk total carnitine was 45 +/- 3 mumol/L. With the carnitine content of breast milk remaining stable for greater than or equal to 10 mo, the importance of exogenous carnitine throughout infancy is suggested.

Carnitine↗
PubMedDate not supplied

Plasma carnitine and breast milk carnitine intake in premature infants.

Ten premature infants with a mean gestational age of 29 weeks (range, 27-32) and a mean birth weight of 1,294 g (range, 930-2,300) and without complications at birth were studied during the first 14 days after birth. Their breast milk intake was recorded and the carnitine content determined in each daily portion. During the first week, the daily mean carnitine intake was low and increased to 6-7 mumoles/kg and day during the second week. Breast milk carnitine concentration ranged from 17 to 148 mumoles/L. Plasma carnitine and its derivatives did not change during the observation period. No relationship was found between the individual cumulative breast milk carnitine intake and total plasma carnitine levels or between carnitine and its derivatives and nonesterified fatty acids or 3-OH-butyrate. The urinary carnitine excretion, in millimoles of carnitine per mole of creatinine, was higher during the second week. In other studies, declining plasma carnitine levels have been observed in premature infants on total parenteral nutrition. The results from this study indicated that premature infants without complicating disorders were able to maintain their plasma carnitine levels.

3-Hydroxybutyric Acid↗
PubMedDate not supplied

Plasma carnitine levels and urinary carnitine excretion during sepsis.

Carnitine is an indispensable factor for the beta-oxidation of medium- and long-chain fatty acids, and it plays a possible role in the oxidation of branched-chain amino acids. Plasma and urinary levels of free carnitine and short-chain acyl-carnitines were studied in 67 surgical patients, after non-septic surgical procedures or during sepsis. The septic state was associated with increased urinary excretion of free carnitine (p less than 0.001), as well as with lower plasma levels of short-chain acyl-carnitines (p less than 0.001); the latter feature correlated with the level of hypermetabolism, as evaluated by the metabolic rate and by the arterial-mixed venous O2 difference. In 26 patients during total parenteral nutrition D, L-acetyl-carnitine was administered (100 mg/kg/24 hrs, in continuous iv infusion) and was associated, in septic patients only, with a significant decrease in the respiratory quotient, suggesting enhanced oxidation of low respiratory quotient substrates (fatty acids and/or branched-chain amino acids). Carnitine supplementation during total parenteral nutrition might be of theoretical benefit in some clinical conditions, such as sepsis, in which the following conditions coexist enhanced utilization of substrates whose oxidation is partially or totally carnitine dependent; prolonged absence of exogenous intake of carnitine (as in long-term total parenteral nutrition); eventual impairment of carnitine synthesis due to hepatic dysfunction; increased, massive urinary loss of carnitine.

Acetylcarnitine↗
PubMed1986

Studies on the effects of L-thyroxine, L-carnitine and an L-thyroxine-L-carnitine combination on dipalmitoyl phosphatidylcholine content and on phosphatidylcholine species composition in fetal rat lungs.

The aim of the present study was to examine the effects of maternal carnitine treatment combined with thyroxine, a hormone influencing both lung maturation and carnitine metabolism. Administration of a carnitine-thyroxine combination to pregnant rats resulted in a significant increase of DPPC content in fetal rat lungs to 8.8 +/- 1.8 mg/g dry weight (mean +/- SD), compared with the control group, the carnitine-treated group, and the thyroxine-treated group [5.4 +/- 1.8 (p less than 0.01), 5.6 +/- 1.5 (p less than 0.01), and 6.6 +/- 1.0 mg/g dry weight, respectively]. The portion of DPPC in the PC species increased significantly from 20.9 +/- 2.1% in the control group and to 27.2 +/- 3.5% (p less than 0.01) in the carnitine-thyroxine combination group. A significant (p less than 0.01) diminution of the palmitoyl-palmitoleyl PC (16:0/16:1-PC) portion in the PC species was found. Maternal carnitine administration resulted in an elevation of the carnitine levels in the fetal lungs to approximately twice those of the controls (p less than 0.01). The combined administration of carnitine and thyroxine resulted in no increase in the total carnitine content but in a significant (p less than 0.01) increase of the short chain acylcarnitine content. The present results demonstrate that carnitine potentiates the effects of thyroxine on DPPC content and support the concept of an interrelationship between carnitine and thyroxine metabolism.

1,2-Dipalmitoylphosphatidylcholine↗