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J L Beard

Publications and source records attributed to J L Beard.

At least 37 records · Page 2Linked to original sources
PubMed1999

A genetic developmental model of iron deficiency: biological aspects.

Numerous studies have demonstrated the negative impact of iron deficiency on growth and development. The present study expands on the published literature by exploring the role of genetics and developmental timing on the impact of iron deficiency on development in two strains of mice. Growth rates, organ weights, and hematological responses to an iron-deficient diet differed by strain and sex. The results from this study provided novel insight into iron metabolism and the impact of iron deficiency in C57 and DBA strains of mice. Future studies should continue to examine the contributions of both genetics and sex to the development of iron deficiency.

Animals↗
PubMed1999

Effects of an omnivorous diet compared with a lactoovovegetarian diet on resistance-training-induced changes in body composition and skeletal muscle in older men.

BACKGROUND: Very limited data suggest that meat consumption by older people may promote skeletal muscle hypertrophy in response to resistance training (RT). OBJECTIVE: The objective of this study was to assess whether the consumption of an omnivorous (meat-containing) diet would influence RT-induced changes in whole-body composition and skeletal muscle size in older men compared with a lactoovovegetarian (LOV) (meat-free) diet. DESIGN: Nineteen men aged 51-69 y participated in the study. During a 12-wk period of RT, 9 men consumed their habitual omnivorous diets, which provided approximately 50% of total dietary protein from meat sources (beef, poultry, pork, and fish) (mixed-diet group). Another 10 men were counseled to self-select an LOV diet (LOV-diet group). RESULTS: Maximal strength of the upper- and lower-body muscle groups that were exercised during RT increased by 10-38% (P < 0.001), independent of diet. The RT-induced changes in whole-body composition and skeletal muscle size differed significantly between the mixed- and LOV-diet groups (time-by-group interactions, P < 0. 05). With RT, whole-body density, fat-free mass, and whole-body muscle mass increased in the mixed diet group but decreased in the LOV- diet group. Type II muscle fiber area of the vastus lateralis muscle increased with RT for all men combined (P < 0.01), and the increase tended to be greater in the mixed-diet group (16.2 +/- 4.4 %) than in the LOV diet group (7.3 +/- 5.1%). Type I fiber area was unchanged with RT in both diet groups. CONCLUSION: Consumption of a meat-containing diet contributed to greater gains in fat-free mass and skeletal muscle mass with RT in older men than did an LOV diet.

Aged↗
PubMed1999

Iron deficiency in young rats alters the distribution of vitamin A between plasma and liver and between hepatic retinol and retinyl esters.

We assessed whether iron deficiency alters the concentration of vitamin A (VA) in plasma or liver and the chemical distribution between hepatic unesterified and esterified retinol. Weanling male Sprague-Dawley rats (n = 10/group) were allocated to one of four diet groups: low iron (ID3, 3 mg of elemental iron/kg diet), marginal iron (ID15, 15 mg/kg), control diet food-restricted to the ID3 group (FR, 35 mg/kg), and control diet ad libitum consumption (AD, 35 mg/kg). Both ID3 and FR rats grew less than AD and ID15 rats. At the end of 5.5 wk, plasma retinol concentrations of the ID3 and FR rats were reduced >40% compared to ID15 and AD rats [Kruskal-Wallis test (K-W), P < 0.0042)]. Paradoxically, the hepatic VA concentration was greater in FR rats, with accumulation of more retinyl esters and retinol compared to the other dietary groups. Concentrations of hepatic retinyl esters and retinol did not differ among the other groups, but the molar ratio of hepatic retinyl esters to retinol was greater in ID3 rats (20.1 +/- 1.4) compared to ID15 rats (13.8 +/- 1.6, P = 0.02), AD (11.3 +/- 2.1, P < 0.0042) and FR (9.5 +/- 1.1, P < 0.0042). Iron deficiency may cause changes in liver and plasma VA that are refractory to VA intake, and thus a benefit may be derived from combining iron and VA supplements during nutrition interventions.

Animals↗
PubMed1999

Iron deficiency and neural development: an update.

In Latin America, 10-30% of reproductive age females and upwards of 40-70% of pregnant women may be iron deficient. The true prevalence in young children and infants is often hard to determine because of problems in survey design, data collection, or sampling. There is little doubt, however, that iron deficiency anemia is a significant nutritional problem in many infants within the first 5 years of life. Numerous intervention studies have been performed across the world with varying success and it is clear that in nearly all situations it is a preventable disease with preventable consequences. One such consequence is the alteration in cognition that occurs in iron deficient individuals during the early parts of their life cycle and perhaps at later times as well. While iron deficiency was once presumed to exert most of its deleterious effects only if anemia was present, it is now clear that many organs show morphologic, physiologic, and biochemical changes before there is any drop in hemoglobin concentration. Iron deficiency is associated with alterations in many metabolic processes that may impact brain functioning; among them are mitochondria electron transport, neurotransmitter synthesis and degradation, protein synthesis, organogenesis, and others. It is necessary to separate the developmental aspects of iron deficiency and neural functioning from the aspects of iron deficiency that could occur at any time in life. A number of reviews have discussed the links between brain iron and neuropathology, brain iron, nutrition, and development, and iron status and cognition. New knowledge concerning the acquisition of iron by the brain in early life is being generated by numerous research groups. In the next decade a much clearer understanding of the role of brain iron on neural functioning will probably emerge.

Animals↗
PubMed1998

Selective ablation of human T-cell lymphotropic virus type 1 p12I reduces viral infectivity in vivo.

Human T-cell lymphotropic virus type 1 (HTLV-1) is the etiologic agent of adult T-cell leukemia and HTLV-1-associated myelopathy. Novel, yet conserved RNA transcripts encoded from open reading frames (ORFs) I and II of the viral pX region are expressed both in vitro and in infected individuals. The ORF I mRNA encodes the protein p12(I), which has been shown to localize to cellular endomembranes, cooperate with bovine papillomavirus E5 in transformation, as well as bind to the IL-2 receptor beta and gamma chains and the H+ vacuolar ATPase. It is unknown what role p12(I) plays in the viral life cycle. Using an infectious molecular clone of HTLV-1 (ACH) and a derivative clone, ACH.p12(I), which fails to produce the p12(I) message, we investigated the importance of p12(I) in infected primary cells and in a rabbit model of the infection. ACH.p12(I) was infectious in vitro as shown by viral passage in culture and no qualitative or quantitative differences were noted between ACH and ACH.p12(I) in posttransfection viral antigen production. However, in contrast to ACH, ACH.p12(I) failed to establish persistent infection in vivo as indicated by reduced anti-HTLV-1 antibody responses, failure to demonstrate viral p19 antigen production in peripheral blood mononuclear cell (PBMC) cultures, and only transient detection of provirus by polymerase chain reaction in PBMC from ACH.p12(I)-inoculated rabbits. These results are the first to show the essential role of HTLV-1 p12(I) in the establishment of persistent viral infection in vivo and suggest potential new targets in antiviral strategies to prevent HTLV-1 infection.

Animals↗
PubMed1998

Transferrin response in normal and iron-deficient mice heterozygotic for hypotransferrinemia; effects on iron and manganese accumulation.

Hypotransferrinemia is a genetic defect in mice resulting < 1% of normal plasma transferrin (Tf) concentrations; heterozygotes for this mutation (+/hpx) have low circulating Tf concentrations. These mice provide a unique opportunity to examine the developmental pattern and response of Tf to iron-deficient diets, and furthermore, to address the controversial role of Tf in Mn transport. Twenty-three weanling +/hpx mice and forty-five wild-type BALB/cJ mice were either killed at weaning or fed diets containing either 13 or 72 mg kg-1 Fe, and killed after four or eight weeks. Plasma Tf concentrations were lower in +/hpx mice, plasma Tf nearly doubled and liver Tf was only 50% of normal in response to iron deficiency. Brain iron concentration did not correlate significantly with either plasma Tf or TIBC. However, iron accumulation into brain continued with iron deficiency whereas most other organs had less iron. These results imply that either there is a selected targeting of iron to the brain by plasma Tf or there is an alternative iron delivery system to the brain. Furthermore, we observed no differences in tissue distribution of 54Mn despite the differences in circulating Tf concentrations and body iron stores; this suggests that there are non-Tf dependent mechanisms for Mn transport.

Animals↗
PubMed1998

Plasma thyroid hormone kinetics are altered in iron-deficient rats.

Iron deficiency anemia is associated with lower plasma thyroid hormone concentrations in rodents and, in some studies, in humans. The objective of this project was to determine if plasma triiodothyronine (T3) and thyroxine (T4) kinetics were affected by iron deficiency. Studies were done at a near-thermoneutral temperature (30 degrees C), and a cool environmental temperature (15 degrees C), to determine plasma T3 and T4 kinetics as a function of dietary iron intake and environmental need for the hormones. Weanling male Sprague-Dawley rats were fed either a low Fe diet [iron-deficient group (ID), <5 microg/g Fe] or a control diet [control group (CN), 35 microg/g Fe] at each temperature for 7 wk before the tracer kinetic studies. An additional ID group receiving exogenous thyroid hormone replacement was also used at the cooler temperature. For T4, the disposal rate was >60% lower (89 +/- 6 vs. 256 +/- 53 pmol/h, P < 0.001) in ID rats than in controls at 30 degrees C, and approximately 40% lower (192 +/- 27 vs. 372 +/- 26 pmol/h, P < 0.01) in ID rats at 15 degrees C. Exogenous T4 replacement in a cohort of ID rats at 15 degrees C normalized the T4 concentration and the disposal rate. For T3, the disposal rate was significantly lower in ID rats in a cool environment (92 +/- 11 vs. 129 +/- 11 pmol/h, P < 0.01); thyroxine replacement again normalized the T3 disposal rate (126 +/- 12 pmol/h). Neither liver nor brown fat thyroxine 5'-deiodinase activities were sufficiently different to explain the lower T3 disposal rates in iron deficiency. Thus, plasma thyroid hormone kinetics in iron deficiency anemia are corrected by simply providing more thyroxine. This suggests a central regulatory defect as the primary lesion and not peripheral alterations.

Anemia, Iron-Deficiency↗
PubMed1998

Dietary iron deficiency results in cardiac eccentric hypertrophy in rats.

This study reports the presence of eccentric cardiac hypertrophy in rats made anemic by feeding an iron-deficient diet. Male weanling Sprague-Dawley rats were provided free access to diets either adequate (n=9) or inadequate in iron (n=8) for a period of 7 weeks from weanling or until 10 weeks of age. At that time, blood was obtained for hematocrit and hemoglobin determination, and liver and hearts were collected for further analysis. Liver non-heme iron levels confirmed that the rats were iron-deficient, and the very low hematocrit and hemoglobin values revealed the presence of physiological anemia. Despite the lighter body weights in the iron-deficient rats, this group had greater absolute heart weights and heart:body weight, clearly demonstrating the presence of cardiac hypertrophy. Iron-deficient rats had elevated heart rates but lower norepinephrine levels than control rats. Sagittal sectioning of all hearts allowed for the measurements of the wall thicknesses, lumen volume, and width dimensions. Results revealed significantly greater left ventricular lesser diameter, apical thickness, and left ventricular volume in hearts from iron-deficient rats compared to iron-adequate rats. The hypertrophy pattern present in iron-deficiency anemia is in contrast to other nutritional models of hypertrophy, such as copper-deficiency, where a concentric hypertrophy occurs both in the presence and absence of anemia.

Anemia, Iron-Deficiency↗
PubMed1997

Regional distribution of iron, transferrin, ferritin, and oxidatively-modified proteins in young and aged Fischer 344 rat brains.

Iron dysregulation in the brain is thought to contribute to the oxidative damage seen in neurodegenerative diseases including Alzheimer's disease and Parkinson's disease. A role for iron in the oxidative stress thought to contribute to normal ageing is less certain. To better characterize the role of iron in normal ageing, the concentrations of iron, transferrin, ferritin, and protein carbonyl groups are measured in nine separate regions of Fischer 344 rats. The largest (approximately 30%) age-related increases in brain iron concentration are seen in the temporal cortex, medial septum, and cerebellum. Ferritin concentration in these same brain regions increases 50 to 250% with age, while protein carbonyl concentration is only -27 to +4%, of young rats. These results indicate that an increase in the major iron-binding protein ferritin compensates for any age-related increase in iron concentration, and suggest that the increased ferritin is cytoprotective, serving to prevent the accumulation of protein carbonyl groups (a principal product of metal-catalysed oxidation of proteins).

Aging↗
PubMed1997

Chromium picolinate supplementation and resistive training by older men: effects on iron-status and hematologic indexes.

Chromium competes with iron for binding to transferrin, and high-dose chromium supplementation has been hypothesized to adversely affect iron status. This study examined the effects of chromium picolinate supplementation on hematologic indexes and selected indexes of iron status in 18 men aged 56-69 y who participated in an introductory resistive training program. The men were randomly assigned (double-blind design) to groups (n = 9) that consumed either 17.8 mumol Cr/d (924 micrograms Cr/d) as chromium picolinate or a low-chromium placebo for 12 wk while engaging in resistive training twice weekly (3 sets of 8-12 repetitions at 80% of one repetition maximum for 5 exercises). Hematocrit, hemoglobin, red blood cell (erythrocyte) count, mean corpuscular volume, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, red blood cell distribution width, platelet count, and mean platelet volume were within normal clinical ranges and were unchanged by either chromium picolinate supplementation or resistive training. Resistive training decreased total-iron-binding capacity from 38.4 +/- 9.3 to 27.3 +/- 5.6 mumol/L (P < 0.0001) and increased transferrin saturation from 35.7 +/- 16.3% to 45.4 +/- 16.9% (P = 0.050). Chromium picolinate supplementation did not influence these responses. Serum iron concentrations and serum ferritin concentrations were unchanged by either resistive training or chromium picolinate supplementation. These data suggest that high-dose chromium picolinate supplementation for 12 wk did not influence hematologic indexes or indexes of iron metabolism or status in older men. The decrease in total-iron-binding capacity and increase in transferrin saturation (%) with resistive training are largely opposite to changes associated with iron depletion and suggest a novel effect of resistive training on iron transport.

Aged↗
PubMed1997

Regional brain iron, ferritin and transferrin concentrations during iron deficiency and iron repletion in developing rats.

Iron deficiency in young rats leads to a decrease in brain iron and ferritin concentrations, an increase in transferrin (Tf) concentration, and an increased rate of uptake of iron from the plasma pool. We conducted two experiments to determine whether brain iron, Tf and ferritin respond quickly to iron repletion and to determine whether brain regions respond heterogeneously. Weanling male Sprague-Dawley rats were fed an iron-deficient diet (<5 mg/kg Fe) for 2 wk followed by an iron-adequate diet (REPL group, 35 mg/kg Fe in Experiment 1 and 15 mg/kg Fe in Experiment 2) for 2 or 4 wks, respectively. Age-matched iron-deficient (ID) and control rats composed the other two groups. Fourteen days of repletion with 35 mg/kg Fe dietary treatment were adequate to normalize hematology, brain microsomal and cytosolic Fe and brain ferritin (Experiment 1). Brain transferrin concentrations in REPL rats, however, were significantly above the levels of controls. Regional brain iron decreased heterogeneously due to dietary iron deficiency (Experiment 2), with some regions having a propensity to keep iron (e.g., substantia nigra, pons, and thalamus) and others losing significant amounts of iron (cortex and hippocampus). Ferritin and Tf concentrations also varied significantly across brain regions in ID and control rats. The hippocampus had the most dramatic Tf response to iron deficiency with elevations of approximately 100%, whereas other regions, except striatum, were unaffected. The brain of developing rats thus distributes iron and iron regulatory proteins differently from the brain of adult rats and is quite avid in its reacquisition of iron during iron therapy.

Anemia, Iron-Deficiency↗
PubMed1997

In vivo dopamine metabolism is altered in iron-deficient anemic rats.

Previous studies of dopamine metabolism in iron-deficient rats demonstrated an elevation in extraneuronal levels of dopamine and a depression in the number of dopamine D2 receptors; however, the importance of anemia per se and the reversibility of these observations are not completely resolved. The purpose of this study was to determine if in vivo reuptake of caudate dopamine is altered by iron deficiency anemia, if it is reversible with iron therapy, and if anemia per se produced the same effects on dopamine metabolism. Male Sprague-Dawley rats (21-d old) were fed an iron-deficient diet (4 mg Fe/kg diet) and then iron repleted (5 mg iron dextran), or were fed an iron adequate diet (35 mg Fe/kg diet) and then given phenylhydrazine to induce hemolytic anemia. In vivo microdialysis was performed in steady-state conditions both before and after iron or no therapy and was followed by an intraperitoneal injection of a dopamine reuptake blocker (cocaine-HCl 30 mg/kg). Thirty percent higher extracellular dopamine levels in the caudate-putamen were observed in iron-deficient rats compared with control rats, but no differences were observed in tissue levels. Hemolytic anemic and iron-repleted rats had normal extracellular dopamine levels. The response to dopamine reuptake blockade was significantly attenuated in iron-deficient rats compared with control, iron-repleted, or hemolytic anemic rats. These experiments provide evidence that iron deficiency blunts the dopamine reuptake mechanism, that this is a reversible process in postweaning rats, and that anemia per se does not cause the increased extracellular dopamine levels.

Anemia, Hemolytic↗
PubMed1997

Age, fitness, and regional blood flow during exercise in the heat.

During dynamic exercise in warm environments, the requisite increase in skin blood flow (SkBF) is supported by an increase in cardiac output (Qc) and decreases in splanchnic (SBF) and renal blood flows (RBF). To examine interactions between age and fitness in determining this integrated response, 24 men, i.e., 6 younger fit (YF), 6 younger sedentary (YS), 6 older fit (OF), and 6 older sedentary (OS) rested for 50 min, then exercised at 35 and 60% maximal O2 consumption (VO2max) at 36 degrees C ambient temperature. YF had a significantly higher Qc and SkBF than any other group during exercise, but fitness level had no significant effect on any measured variable in the older men. At 60% VO2max, younger subjects had significantly greater decreases in SBF and RBF than the older men, regardless of fitness level. Total flow redirected from these two vascular beds (deltaSBF + deltaRBF) followed YF >> YS > OF > OS. A rigorous 4-wk endurance training program increased exercise SkBF in OS, but deltaSBF and deltaRBF were unchanged. Under these conditions, older men distribute Qc differently to regional circulations, i.e., smaller increases in SkBF and smaller decreases in SBF and RBF. In younger subjects, the higher SkBF associated with a higher fitness level is a function of both a higher Qc and a greater redistribution of flow from splanchnic and renal circulations, but the attenuated splanchnic and renal vasoconstriction in older men does not appear to change with enhanced aerobic fitness.

Adult↗
PubMed1997

A sustainable solution for dietary iron deficiency through plant biotechnology and breeding to increase seed ferritin control.

OBJECTIVES: To stimulate novel sustainable solutions to the problem of the nutritional iron deficiency, we asked: How does Nature insure proper iron nutrition of embryos and neonatal animals? Estimates of iron deficiency world-wide are 30% of the population, with women and children at the greatest risk. Recent studies linking iron deficiency with impeded cognitive development emphasizes the enormity of the impact of iron deficiency. Sustainable solutions to the problem of dietary iron deficiency have been elusive. RESULTS: Data for storage iron was examined in seeds, developing plants, embryos and developing animals. In all cases, the common source of stored iron for development was ferritin. The protein component of ferritin concentrates iron billions of times above the solubility of the free metal ion. High conservation of ferritin sequences in bacteria, plants and animals and the specificity of ferritin bioavailability either added extrinsically or intrinsically enriched in a selected soybean cultivar, showed high efficacy in curing dietary iron deficiency in the rat model. Older data on ferritin were reevaluated in light of contemporary knowledge. CONCLUSIONS: Enhancement of natural seed ferritin content by biotechnology and breeding has the potential for a sustainable solution to the problem of global dietary iron deficiency.

Animals↗
PubMed1996

The role of nutrition in the development of normal cognition.

The goal of this section of the meeting was to review the relation between nutrition and cognition. The topics selected for discussion included generalized malnutrition, iodine deficiency, iron metabolism, and the relation of fatty acids to the development of the nervous system. Each subject is immense and demands a detailed exposition, but can be treated here only in brief form. However, these short essays should give some insight into the status of our current knowledge.

Brain↗
PubMed1996

Purified ferritin and soybean meal can be sources of iron for treating iron deficiency in rats.

Ferritin and soybean meal were reevaluated as dietary treatments of iron deficiency in rats. Isotopes that had been used in the past were avoided because of contemporary knowledge of the physiological and structural complexity of ferritin protein and the solid iron mineral. Rats made anemic by iron-deficient diets were given equivalent amounts of iron as FeSO4, horse spleen ferritin, baked soybean meal, or soybean meal plus ferritin. Full recovery (89-109%) from anemia and increased tissue iron occurred after 28 d of treatment with any of the iron sources, which contrasts to past bioavailability studies using 59Fe-labeled ferritin and generally shorter periods of observation. Cultivar-specific variability was observed in soybean seed soluble iron and ferritin content (1.9-2.0 times the control cultivar, Arksoy), which was apparently heritable. The combined data suggest that manipulating ferritin expression and other soluble components of seed iron in soybeans and possibly other seeds, using Mendelian and biotechnological approaches, could contribute to a sustainable solution to global problems of iron deficiency.

Anemia, Iron-Deficiency↗
PubMed1996

Iron metabolism: a comprehensive review.

Despite its abundance in the earth's crust, iron deficiency is a serious health issue in many parts of the world. Although fundamental observations about iron metabolism and the significance of iron nutriture were first noted some time ago, the molecular mechanisms involved in iron metabolism are just now being defined.

Animals↗