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Biomedical subjects

P R Borum

Publications and source records attributed to P R Borum.

At least 19 recordsLinked to original sources
PubMed1994

A phase I/II trial of intravenous L-2-oxothiazolidine-4-carboxylic acid (procysteine) in asymptomatic HIV-infected subjects.

Twenty-four asymptomatic, HIV-1-seropositive subjects with CD4 cell counts of > or = 400/microliters participated in a Phase I/II, dose escalation trial of intravenous L-2-oxothiazolidine-4-carboxylic acid (OTC: Procysteine). Four groups of six subjects each were consecutively assigned to receive OTC at an initial dose of 3, 10, 30, or 100 mg/kg, followed by the same dose given twice weekly for 6 weeks. Increases in whole-blood glutathione were observed in the highest dosage group after 6 weeks of therapy. No effects on changes in CD4 cell counts, viral load, or proviral DNA frequency were observed among the four dosage groups, although a decline in beta 2-microglobulin levels was apparent in the highest dosage group. One subject withdrew due to headaches; other probable adverse events including rash, flushing, pruritus, lightheadedness, and diminished concentration were self-limited.

Adult↗
PubMed1992

Medium-chain triglycerides in formula for preterm neonates: implications for hepatic and extrahepatic metabolism.

Medium-chain fatty acids are an important energy source for preterm neonates. Based on assumptions from earlier investigations, 40% to 60% of fatty acids in formula designed for preterm neonates are C6:0 to C12:0. This review will reevaluate these assumptions about C6:0 to C12:0 fatty acids. More recent investigations have indicated that when C6:0 to C12:0 fatty acids are administered in high concentrations, they are metabolized in several tissues by carnitine-dependent mechanisms. Incomplete oxidation of C6:0 to C12:0 fatty acids may result in elevated dicarboxylic acid levels. Feeding formulas high in C6:0 to C12:0 fatty acids has not improved nitrogen retention or growth of preterm neonates. Current data indicate that the fatty acid profiles of formula for preterm neonates are not optimal. Optimization of the fatty acid profile in the diet awaits an improved understanding of the metabolism of fatty acids of all chain lengths in the preterm neonate.

Animals↗
PubMed1991

Carnitine and lipid metabolism.

Carnitine, a short-chain nitrogen containing carboxylic acid, is found in meat and dairy foods. Carnitine aids in a shuttle process that makes long-chain, fatty-acid coenzyme A derivatives available for B-oxidation. Normal healthy adults have adequate carnitine stores and do not require dietary carnitine. However, neonates, chronically and critically ill patients with decreased muscle and liver carnitine store seem to benefit from carnitine supplementation to enhance their tolerance of metabolic stress.

Carnitine↗
PubMed1989

Creation of a regional medical-nutrition education network.

The Southeastern Regional Medical-Nutrition Education Network (SER-MEN) was developed to coordinate and improve nutrition education in a consortium of the medical schools in Alabama, Florida, Georgia, and South Carolina. SERMEN's central office is at the Medical College of Georgia with the testing office at the University of Alabama at Birmingham. Students, faculty, and consultants in nutrition, education, and computer networking work together on projects on each campus that are coordinated and planned through semiannual meetings. A standardized examination was developed with the Nutrition Test-Item Bank to assess nutrition knowledge at various years of medical students from network schools. Each SERMEN school is connected to a microcomputer system at the central office that provides access to a data base of nutrition education and resources on each campus for developing curricula and syllabi. Funding has been provided by societies, foundations, and government agencies.

Computer Communication Networks↗
PubMed1989

Blood carnitine status after orthotopic liver transplantation in patients with end-stage liver disease.

We determined the effects of orthotopic liver transplantation on plasma and red cell carnitine concentrations in patients with end-stage liver disease. Before transplantation, plasma and red cell carnitine were significantly elevated above normal. The partitioning factor (ratio of red cell carnitine to plasma carnitine) was four times greater than that observed in our reference population. After hepatic replacement, plasma and red cell carnitine approached normal levels within 6 mo. The partitioning factor, however, remained elevated at that time. These results indicate that 1) there is no evidence for carnitine deficiency in severe liver disease on the basis of carnitine concentrations in the plasma and red compartments and 2) altered partitioning of carnitine between plasma and red cells persists for greater than or equal to 6 mo after hepatic replacement.

Carnitine↗
PubMed1988

Fatty acid oxidation in the myocardium: effects of parathyroid hormone and CRF.

Fatty acids constitute an important substrate utilized by the myocardium as a major fuel for energy production; certain data suggest that oxidation of long chain fatty acids (LCFA) may be impaired in uremia, and such a derangement could, in part, contribute to the myocardiopathy of uremia. The latter is associated with secondary hyperparathyroidism and PTH has been shown to affect myocardial metabolism. The present study evaluated in rats the effects of four days administration of PTH and 21 days of chronic renal failure (CRF) with and without excess PTH on oxidation of alpha-ketoglutarate, beta-hydroxybutyric acid, LCFA and short chain fatty acids (SCFA). PTH impaired oxidation of alpha-ketoglutarate, LCFA, SCFA, but not of beta-hydroxybutyric acid and reduced the activity of carnitine palmitoyl transferase (CPT). Inactivation of the PTH abolished its effects. CRF rats with intact parathyroid glands also had impaired oxidation of LCFA and CTP activity. Carnitine contents of myocardium were not altered. The data show that PTH excess in normal rats is associated with impaired oxidation of LCFA and SCFA, and secondary hyperparathyroidism in CRF animals impairs oxidation of LCFA. This effect is due to: 1) reduction in the activity of CPT, a key enzyme for the transport of LCFA to mitochondrial matrix for beta-oxidation; and 2) impairment in beta-oxidation. The data provide for new and additional pathway through which excess PTH and CRF can affect myocardial metabolism.

Animals↗
PubMed1988

Chronic renal failure, parathyroid hormone and fatty acids oxidation in skeletal muscle.

Fatty acids are an important source of skeletal muscle energy, and certain data suggest oxidation of long-chain fatty acids (LCFA) may be impaired in uremia. This abnormality may in part be responsible for uremic myopathy. Uremia is associated with hyperparathyroidism and PTH affects muscle metabolism; PTH enhances muscle proteolysis and impairs muscle bioenergetics, and it is possible that PTH also affects fatty acids oxidation. The present study examined in rats the effects of 4 days administration PTH and of 21 days of chronic renal failure (CRF) with and without excess PTH on oxidation of LCFA and short-chain fatty acids (SCFA). Both 1-84 and 1-34 PTH impaired oxidation of LCFA but not of a SCFA (beta-hydroxybutyric acid) and reduced the activity of carnitine palmitoyl transferase (CPT). Inactivation of the PTH abolished its effects. CRF rats with intact parathyroid glands had also impaired oxidation of LCFA and of CPT activity. Parathyroidectomy in CRF rats normalized these abnormalities. Carnitine contents of muscle were not altered. The data show that PTH excess in normal or in CRF rats is associated with impaired oxidation of LCFA and this effect is due to reduction in the activity of CPT, a key enzyme for the transport of LCFA to mitochondrial matrix for beta-oxidation. The data demonstrate another toxic effect of PTH on muscle in CRF and provide an additional pathogenic mechanism for uremic myopathy.

Animals↗
PubMed1988

Cross-sectional study of nutrition knowledge and attitudes of medical students at three points in their medical training at 11 southeastern medical schools.

Eleven southeastern medical schools cooperated to evaluate nutrition knowledge and attitudes of medical students. This study complements previous reports of an examination of entering freshmen and seniors. Average knowledge scores for 165 students tested after basic sciences (preclinical) training in this study were 67 +/- 7% compared with 53 +/- 6% for freshmen and 69 +/- 8% for seniors. The upperclassmen's scores were higher than the freshmen's (p less than 0.001) and varied with the amount of required nutrition teaching. Only 13% of preclinical students perceived nutrition as important to their careers compared with 74% of entering and 59% of graduating students, suggesting that preclinical teaching reduces their sense of relevance of nutrition to medicine. These findings suggest that nutrition knowledge can be increased through preclinical coursework and that the knowledge level can be maintained through the clinical years. However, the positive attitude of freshmen toward nutrition is lost after preclinical training and is only partially regained after the clinical years.

Attitude of Health Personnel↗
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↗