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Biomedical subjects

P R Borum

Publications and source records attributed to P R Borum.

At least 37 records · Page 2Linked to original sources
PubMed1987

Plasma carnitine compartment and red blood cell carnitine compartment of healthy adults.

Carnitine is needed for a variety of important physiological functions in energy metabolism. Assessment of the carnitine status of an individual is compromised by limited data on the number of metabolic compartments of carnitine and their interrelationship, if any. Possible compartmentalization of carnitine in the blood of healthy adults was investigated because blood is one of the more readily available samples for the assessment of carnitine status. The data suggest that blood carnitine is partitioned into a plasma carnitine compartment and a red blood cell carnitine compartment, compartments that are separate and distinct metabolic compartments.

Adolescent↗
PubMed1987

The neonatal piglet as a model for human neonatal carnitine metabolism.

Investigations concerning carnitine metabolism and possible requirements for exogenous carnitine in human preterm neonates are limited by ethical considerations. The neonatal piglet is a potential animal model for these investigations. Tissue carnitine concentrations were determined in fetuses from cross-bred domestic gilts at stages of gestation corresponding to those of neonates found in neonatal intensive care units. Fetal piglet plasma and red blood cell carnitine levels decreased from approximately 90 d to term. Skeletal muscle carnitine increased from 60 d to term. Temporal changes in fetal carnitine concentrations in plasma, red blood cells and skeletal muscle throughout gestation are similar to the pattern reported by our laboratory for the human neonate. Cardiac muscle carnitine increased earlier than skeletal muscle but also continued to increase to term. Carnitine concentrations in fetal liver, kidney and intestine were maximal at 90 d and decreased until term. Similarities in physiology, metabolism and profiles of tissue carnitine concentration between the newborn piglet and the human neonate indicate that the neonatal piglet is an appropriate animal model for investigations concerning neonatal carnitine metabolism.

Animals↗
PubMed1986

Enhanced lipid utilization in infants receiving oral L-carnitine during long-term parenteral nutrition.

Fourteen infants requiring long-term total parenteral nutrition but able to tolerate small quantities of enteral feedings were randomized into carnitine treatment and placebo control groups. All infants had received nutritional support devoid of carnitine. Plasma carnitine levels and observed plasma lipid indices were not different before supplementation. Under standardized, steady-state conditions, 0.5 g/kg fat emulsion (intralipid) was administered intravenously over 2 hours both before and after infants received 7 days of continuous nasogastric or gastric tube L-carnitine (50 mumol/kg/day) or placebo. Plasma triglyceride, free fatty acid, acetoacetate, beta-hydroxybutyrate, and carnitine concentrations were observed at 0 (start of lipid infusion), 2, and 4 hours for pre- and post-treatment periods, and in addition at 6 and 8 hours after carnitine supplementation. Infants receiving carnitine had significantly greater beta-hydroxybutyrate plasma concentrations (P less than 0.05) and carnitine (P less than 0.001) at 0, 2, 4, 6, and 8 hours, and greater plasma acetoacetate concentrations (P less than 0.05) at 2, 4, 6, and 8 hours, compared with controls. Twenty-four-hour urinary carnitine excretion was very low for both groups before supplementation; after supplementation, excretion was higher (P less than 0.05) in the carnitine group. No significant differences were found between groups for plasma triglyceride or free fatty acid concentrations at any observation period. This study demonstrated enhanced fatty acid oxidation, as evidenced by increased ketogenesis, with L-carnitine supplementation in infants receiving long-term total parenteral nutrition.

3-Hydroxybutyric Acid↗
PubMed1986

Carnitine as an essential nutrient.

Carnitine performs a critically important role in energy metabolism and is synthesized in the healthy adult predominantly in the liver and kidney. The typical well balanced American diet contains significant amounts of carnitine as well as the essential amino acids and micronutrients needed for carnitine biosynthesis. Thus carnitine is an infrequent problem in the healthy, well nourished adult population in the United States. However, carnitine can be a conditionally essential nutrient for several different types of individuals. Preterm infants require carnitine for life-sustaining metabolic processes but have a carnitine biosynthetic capability that is not fully developed. There is an increasing number of documented problems with carnitine metabolism in preterm infants not receiving an exogenous source of carnitine indicating that endogenous biosynthesis of carnitine is not adequate to meet the infant's need. Children with different forms of organic aciduria appear to have a greatly increased need for carnitine to function in the excretion of the accumulating organic acids. This need exceeds their dietary carnitine intake and carnitine biosynthetic capability. Renal patients treated with chronic hemodialysis appear to lose carnitine via the hemodialysis treatment, and this loss cannot be repleted simply by endogenous biosynthesis and dietary intake. Treatment with drugs such as valproic acid and metabolic stresses such as trauma, sepsis, organ failure, etc, can also result in a requirement for exogenous carnitine. Accurate assessment of the carnitine status of patients at risk for carnitine deficiency is fundamental to the identification of those patients who require carnitine as the result of altered metabolism.

Adult↗
PubMed1986

Carnitine nutriture of dialysis patients.

Hemodialysis patients often experience muscle weakness, cardiac arrhythmias, and hypertriglyceridemia, along with other conditions that may lead to atherosclerosis and coronary heart disease. A contributing factor in the etiology of the symptoms may be carnitine deficiency. Patients undergoing renal dialysis treatment are at risk for developing a carnitine deficiency. The small carnitine molecule can be easily lost into the dialysate. A diseased kidney may lead to a decrease in the endogenous supply of carnitine since the kidney is a major site of carnitine biosynthesis. The diet of dialysis patients may be limiting in preformed carnitine as well as in the precursors and micronutrients required for carnitine biosynthesis. Both oral and intravenous supplementation of L-carnitine have been shown to alleviate muscle weakness, reduce the incidence and severity of arrhythmias, and decrease plasma triglyceride levels, along with alleviating other complications noted in dialysis patients. Health care professionals must be aware of the possible benefits of providing carnitine supplementation for renal dialysis patients.

Arrhythmias, Cardiac↗
PubMed1985

Carnitine concentration of red blood cells.

The presence of significant concentrations of carnitine in red blood cells is documented using an assay procedure that is described in detail. Red blood cells can be prepared for assay by simple techniques and stored frozen. The reproducibility of the assay procedure is within acceptable limits. Usefulness of the procedure in an experimental setting has been documented with an investigation of both plasma and red blood cell carnitine concentrations of rats of different ages. Earlier studies have demonstrated that plasma carnitine concentrations are two-fold higher in adult male rats than in adult female rats. In agreement with that data, the adult male rat has a red blood cell carnitine concentration which is two-fold higher than that of adult female rats.

Aging↗
PubMed1985

Role of carnitine during development.

Fatty acids are an important fuel source for neonates. The utilization of long chain fatty acids as a fuel source is dependent upon adequate concentrations of carnitine. Carnitine also has functions in other physiological processes critical to the survival of the neonate such as lipolysis, thermogenesis, ketogenesis, and possibly regulation of certain aspects of nitrogen metabolism. Plasma and tissue carnitine concentrations in neonates are depressed compared with those of older individuals. The capability for carnitine biosynthesis is much less in the neonate than in the adult. Human milk contains carnitine and appears to be the major source of carnitine to meet the neonate's metabolic needs. However, total parenteral nutrition solutions and soy-based infant formulas contain no carnitine. Evidence is accumulating that all infant diets may need to supply carnitine to meet the neonate's metabolic needs.

Acids↗
PubMed1984

Tissue carnitine reserves of newborn infants.

This study assessed the tissue reserves of carnitine at birth in a group of neonates (n = 22) of varying gestational age dying within 24 h of birth, prior to possible changes in carnitine status induced by postnatal intervention. Tissue carnitine concentration was highest in the muscle in each infant. The mean (+/- SD) muscle carnitine concentration of 8.4 +/- 3.6 nmol/mg noncollagen protein (NCP) in very immature infants (less than or equal to 1000 g birth weight) was significantly lower than the corresponding mean (+/- SD) values of 14.0 +/- 3.2 nmol/mg NCP in larger preterm infants (1001-2500 g; P less than 0.01) and 19.4 +/- 2.6 nmol/mg NCP in term infants (greater than or equal to 2501 g; P less than 0.001). Muscle carnitine concentration correlated positively with gestational age (r = 0.832; P less than 0.001) and with body dimensions. Liver and heart carnitine concentrations did not correlate significantly with gestation or body dimensions. The mean (+/- SD) liver carnitine concentration for all the neonates as a group was 4.1 +/- 1.5 nmol/mg NCP. The mean (+/- SD) heart carnitine concentration was 4.7 +/- 1.3 nmol/mg NCP. In comparison to adult controls, tissue carnitine concentrations were markedly lower in neonates, particularly in immature newborns. These data suggest that newborn infants, especially premature babies, are born with limited tissue reserves of carnitine and are therefore at an increased risk for developing carnitine deficiency and its adverse effects in the postnatal period, particularly if maintained on carnitine-free intravenous nutrition for prolonged periods of time.

Carnitine↗
PubMed1983

Cardiac carnitine deficiency and altered carnitine transport in cardiomyopathic hamsters.

The Bio 14.6 hamster has a well-documented cardiomyopathy which leads to congestive heart failure. Previous work demonstrated that hearts from these hamsters have depressed fatty acid oxidation and depressed carnitine concentrations compared to those of normal hamsters. Analyses of tissue carnitine concentrations from 40 to 464 days of age demonstrate that the cardiomyopathic hamsters have a cardiac carnitine deficiency throughout life. Therefore, the carnitine deficiency is not a secondary effect of an advanced stage of the cardiomyopathy. Both the observation that other tissues of the cardiomyopathic hamster have normal or markedly elevated carnitine concentrations and the observation that oral carnitine treatment could not increase the cardiac carnitine concentrations to those of normal hamsters are consistent with the hypothesis that the cardiac carnitine deficiency is the result of a defective cardiac transport mechanism. Cardiac carnitine-binding protein (which may function in the cardiac carnitine transport mechanism) prepared from hearts of cardiomyopathic hamsters had a lower maximal carnitine binding and an increased dissociation constant for carnitine compared to the cardiac carnitine-binding protein prepared from normal hamsters. Thus, several types of data indicate that the cardiomyopathic hamster has an altered cardiac carnitine transport mechanism.

Animals↗
PubMed1983

Carnitine.

Carnitine has a critical role in energy metabolism. Many of the functions of carnitine are not clearly elucidated and many of the regulatory mechanisms governing carnitine metabolism are ill-defined. Carnitine deficiency can be life threatening but may be resolved with carnitine supplementation. Various groups of individuals in addition to those with the classical carnitine deficiency syndrome may require exogenous carnitine. Carnitine nutriture can no longer be ignored.

Animals↗
PubMed1983

Carnitine status at birth of newborn infants of varying gestation.

This study assessed and compared the plasma and red blood cell concentrations of carnitine in cord blood samples from preterm (less than or equal to 36 wk, n = 53) and term (greater than or equal to 37 wk, n = 72) neonates. The mean (+/- S.E.) plasma carnitine concentration (PL[C]) was significantly higher in preterm than in term neonates (29.0 +/- 1.8 versus 22.4 +/- 0.8 nmole/ml; P less than 0.001). Likewise, the mean (+/- S.E.) red blood cell carnitine concentration (RBC[C]) was significantly higher in preterm than in term neonates (0.24 +/- 0.02 versus 0.14 +/- 0.01 nmole/mg Hgb; P less than 0.001). Both PL[C] and RBC[C] were particularly elevated in extremely immature neonates (less than or equal to 33 wk gestation). Linear regression analysis showed a significantly negative correlation between PL[C] and gestational age (r = -0.332; P less than 0.001), and between RBC[C] and gestational age (r = -0.531; P less than 0.001). Approximately 72.2 +/- 1.1% (mean +/- S.E.) of carnitine in blood was estimated to be contained in the RBC, and 27.8 +/- 1.1% (mean +/- S.E.) of carnitine was estimated to be in the plasma.

Birth Weight↗
PubMed1983

Nonketotic hypoglycemia: an early indicator of systemic carnitine deficiency.

In systemic carnitine deficiency, an early phase of nonketotic hypoglycemia and liver dysfunction may precede a late phase of encephalopathy and myopathy. We studied two children with recurrent episodes of nonketotic hypoglycemia who were found to have systemic carnitine deficiency without myopathy or encephalopathy. Early institution of appropriate therapy prevented the onset of late debilitating complications in one patient, whereas therapeutic noncompliance in the other patient led to an episode of encephalopathy and myopathy. Metabolic studies indicated that decreased availability of alanine may be a factor in the genesis of hypoglycemia; concurrent depletion of cerebral glucose, ketones, and glycogen may be the cause of the encephalopathy.

Brain Diseases↗
PubMed1982

Identification of a cardiac carnitine binding protein.

The existence of a cardiac carnitine binding protein was demonstrated using an in vitro binding assay. The binding activity was solubilized with Triton X-100 from the pellet following a 59,000 X g centrifugation of rat ventricular homogenates. Preincubation at temperatures above 40 degrees C or treatment with pronase significantly reduced the binding activity, suggesting that the activity was that of a protein. Cell fractionation studies suggested that the cardiac carnitine binding protein was associated with the plasma membrane fraction and that its activity was distinct from carnitine palmitoyl-transferase, carnitine acetyltransferase, and carnitine translocase. Optimal binding required 60 min of incubation at 25 degrees C. The binding of carnitine to the cardiac carnitine binding protein was saturable, and a dissociation constant of 0.7 microM for DL-carnitine was measured. L-Carnitine competed with DL-[methyl-3H]carnitine for competition by D-carnitine was much less effective. Binding was significantly inhibited when N-ethylmaleimide, iodoacetic acid, or mercuric chloride was present. Once DL-[3H]carnitine was bound to the cardiac carnitine binding protein, radioactivity could be dissociated by a variety of mild treatments including dialysis, overnight incubation at 4 degrees C, and application to a gel filtration column.

5'-Nucleotidase↗
PubMed1982

Delivery of vitamins E and C from parenteral alimentation solution.

We have previously shown that substantial losses of fat-soluble (FS) vitamin A from parenteral alimentation solution occur due to adsorption in the intravenous tubing and photodegradation in the bottle. This study assessed the delivery of other vitamins, viz, FS vitamin E and water-soluble (WS) vitamin C, from parenteral alimentation solution. The solution containing 2.0 ml/L of an aqueous multivitamin infusion was infused at a constant rate of 10 ml/h using a standard intravenous administration set. Multiple aliquots of the solution from the bottle and the effluent obtained sequentially in a 24-h period were analyzed for concentrations of vitamins E and C. Both vitamins remained relatively stable in the bottle. A significant amount (12%) of vitamin E was lost in the intravenous tubing. No losses of vitamin C were incurred in the intravenous tubing. The data suggest that delivery of FS vitamin E from parenteral alimentation solutions is less than optimum because of adsorptive losses. Similar losses are not encountered with WS vitamin C.

Ascorbic Acid↗
PubMed1981

Dietary-dependent carnitine deficiency as a cause of nonketotic hypoglycemia in an infant.

Recurrent episodes of hypoglycemia, prostration, vomiting, and hepatomegaly were observed in an infant fed a carnitine-free soy formula. The extremely low plasma and urinary carnitine concentrations, elevated plasma free fatty acids, disproportionately low plasma beta hydroxybutyrate, and elevated urinary dicarboxylic acids, in the presence of a fatty liver, suggested that carnitine deficiency was the basis for this child's metabolic disturbance. When the infant was fed an enriched carnitine diet, remarkable clinical, biochemical, and histologic improvement was observed. The possibility that carnitine may be an essential nutrient for some infants is raised by the findings in this patient.

Carnitine↗