Biomedical subjects

William C Heird

Publications and source records attributed to William C Heird.

23 records · Page 2Linked to original sources

PubMed2002

Response of splanchnic and whole-body leucine kinetics to treatment of children with edematous protein-energy malnutrition accompanied by infection.

BACKGROUND: Although the reduction in whole-body protein turnover and net protein loss induced by protein-energy malnutrition (PEM) has been well documented, it is unclear whether the protein-sparing mechanisms elicited by chronically inadequate intakes of dietary protein and energy are affected by the protein catabolic response to infection. OBJECTIVE: The objective of this study was to determine whether the presence of infection alters the PEM-induced reduction in whole-body protein metabolism. DESIGN: We determined whole-body leucine kinetics in 4 boys and 3 girls aged 6-15 mo with edematous PEM and infection approximately 3 d after admission (study 1), when they were both infected and malnourished; approximately 11 d after admission (study 2), when infection had resolved but they were still anthropometrically malnourished; and at recovery (study 3), when weight-for-length was at least 90% of that expected. RESULTS: The children had significantly less leucine flux in both study 1 and study 2 than they had in study 3. There were no significant differences in the amount of leucine released from protein breakdown or used for protein synthesis between study 1 and study 2. There were no significant differences in leucine balance or in either the amount or percentage of enteral leucine extracted by the splanchnic tissues among the 3 studies. CONCLUSIONS: When subjects are in the fed state, severe PEM induces a marked reduction in whole-body protein synthesis and breakdown rates, and the presence of infection does not alter this adaptation and hence the overall protein balance. A corollary is that children with severe PEM do not mount a protein catabolic response to infection.

Deuterium↗

PubMed2002

Cysteine supplementation improves the erythrocyte glutathione synthesis rate in children with severe edematous malnutrition.

BACKGROUND: Children with severe edematous malnutrition have higher than normal oxidant damage and lower concentrations of the antioxidant reduced glutathione (GSH), which are associated with slower synthesis of GSH and with low extra- and intracellular concentrations of the precursor amino acid cysteine. OBJECTIVE: We tested whether early dietary supplementation with cysteine could restore a normal GSH concentration and synthesis rate in these children. DESIGN: Erythrocyte cysteine and GSH concentrations and the fractional and absolute synthesis rates of GSH were measured in 2 groups of 16 edematous malnourished children, 10 boys and 6 girls aged 6-18 mo, at 3 times after hospital admission: at approximately 2 d (period 1), when they were malnourished and infected; at approximately 11 d (period 2), when they were malnourished but cleared of infection; and at approximately 50 d (period 3), when they had recovered. Supplementation with either 0.5 mmol. kg(-1). d(-1) N-acetylcysteine (NAC group) or alanine (control group) started immediately after period 1 and continued until recovery. RESULTS: From period 1 to period 2 the concentration and the absolute synthesis rate of GSH increased significantly (P < 0.05) in the NAC group but not in the control group. The increases in the GSH concentration and synthesis rate were approximately 150% and 510% greater, respectively, in the NAC group than in the control group. The increases in the NAC group were associated with a significant effect of supplement (P < 0.03) on erythrocyte cysteine concentration. CONCLUSION: These results suggest that the GSH synthesis rate and concentration can be restored during the early phase of treatment if patients are supplemented with cysteine.

Acetylcysteine↗

PubMed2002

The acute-phase protein response to infection in edematous and nonedematous protein-energy malnutrition.

BACKGROUND: Immune structure and function are more compromised in edematous protein-energy malnutrition (PEM) than in nonedematous PEM. Whether the positive acute-phase protein (APP) response to infection is affected remains unknown. OBJECTIVE: We assessed whether children with edematous PEM can mount a general APP response and compared the kinetic mechanisms of the response in children with edematous PEM with those in children with nonedematous PEM. DESIGN: Plasma C-reactive protein, alpha(1)-acid glycoprotein, alpha(1)-antitrypsin, haptoglobin, and fibrinogen concentrations and the fractional and absolute synthesis rates of alpha(1)-antitrypsin, haptoglobin, and fibrinogen were measured in 14 children with edematous PEM, aged 11.4 +/- 2 mo, and 9 children with nonedematous PEM, aged 10.1 +/- 1.4 mo, at 3 times: approximately 2 d after hospital admission (period 1), when they were malnourished and infected; approximately 8 d after admission (period 2), when they were malnourished but free of infection; and approximately 54 d after admission (period 3), when they had recovered. RESULTS: Children with edematous and nonedematous PEM had higher plasma concentrations of 4 of 5 APPs in period 1 than in period 3. The magnitude of the difference in concentration and in the rate of synthesis of the individual APPs was less in the children with edematous PEM than in those with nonedematous PEM. The kinetic data show that the characteristics of the APP response were different in the 2 groups. CONCLUSIONS: These results suggest that severely malnourished children can mount only a partial APP response to the stress of infection and that the magnitude of this response is less in those with edema.

Acute-Phase Proteins↗

PubMed2002

The fatty acid profile of buccal cheek cell phospholipids is a noninvasive marker of long-chain polyunsaturated Fatty Acid status in piglets.

The fatty acid pattern of cheek cell phospholipids has been proposed as a noninvasive marker of long-chain polyunsaturated fatty acid (PUFA) status. However, the cheek cell phospholipid fatty acid pattern has been compared only with that of plasma and erythrocytes. The objective of this study was to assess the extent to which the fatty acid profile of cheek cell phospholipids reflects that of tissue phospholipids. Piglets (n = 31; 6 d old) were fed five formula diets differing in total fat and fatty acid composition. After 14 d of consuming the assigned diets, cheek cell plasma, erythrocyte, liver, muscle, adipose tissue, retina and brain samples were collected for determination of the phospholipid fatty acid patterns. There were significant correlations between the cheek cell phospholipid content of most PUFA and the content of these fatty acids in tissue phospholipids (r = 0.509-0.951, P < 0.01). The cheek cell phospholipid content of most of the PUFA, except 20:4(n-6), reflected that of other tissue phospholipids as well as, or nearly as well as the contents of plasma and/or erythrocyte phospholipids. The correlations between the 22:6(n-3) contents of cheek cell, plasma, or erythrocyte phospholipids and those of brain and retina phospholipids were relatively poor (r = 0.596-0.737, P < 0.001). We conclude that the fatty acid pattern of cheek cell phospholipid can be used as a noninvasive marker of PUFA status, but it is not a better index than the pattern of plasma or erythrocyte phospholipids, particularly for assessing the fatty acid pattern of organs with slow fatty acid incorporation and/or turnover rates.

Adipose Tissue↗

PubMed2002

Fatty acid regulation of gene expression: a genomic explanation for the benefits of the mediterranean diet.

The development of obesity and associated insulin resistance involves a multitude of gene products, including proteins involved in lipid synthesis and oxidation, thermogenesis, and cell differentiation. The genes encoding these proteins are in essence the blueprints that we have inherited from our parents. However, what determines the way in which blueprints are interpreted is largely dictated by a collection of environmental factors. The nutrients we consume are among the most influential of these environmental factors. During the early stages of evolutionary development, nutrients functioned as primitive hormonal signals that allowed the early organisms to turn on pathways of synthesis or storage during periods of nutrient deprivation or excess. As single-cell organisms evolved into complex life forms, nutrients continued to be environmental factors that interacted with hormonal signals to govern the expression of genes encoding proteins involved in energy metabolism, cell differentiation, and cell growth. Nutrients govern the tissue content and activity of different proteins by functioning as regulators of gene transcription, nuclear RNA processing, mRNA degradation, and mRNA translation, as well as functioning as posttranslational modifiers of proteins. One dietary constituent that has a strong influence on cell differentiation, growth, and metabolism is fat. The fatty acid component of dietary lipid not only influences hormonal signaling events by modifying membrane lipid composition, but fatty acids have a very strong direct influence on the molecular events that govern gene expression. In this review, we discuss the influence that (n-9), (n-6), and (n-3) fatty acids exert on gene expression in the liver and skeletal muscle and the impact this has on intra- and interorgan partitioning of metabolic fuels.

Dietary Fats, Unsaturated↗