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Biomedical subjects

R R Wolfe

Publications and source records attributed to R R Wolfe.

At least 19 recordsLinked to original sources

Atrial natriuretic peptide and nitric oxide in children with pulmonary hypertension after surgical repair of congenital heart disease.

ANP causes pulmonary vasodilation in some children with pulmonary hypertension secondary to congenital heart disease. In a small group of patients, ANP lowered mean pulmonary artery pressure and pulmonary vascular resistance index > 20% without changing systemic vascular resistance index. Inhaled NO is an effective pulmonary vasodilator and is a more selective pulmonary vasodilator than ANP. The utility of ANP may be limited by its nonselective effects as more selective vasodilator agents are available.

Adolescent

Effect of endurance training on glycerol kinetics during strenuous exercise in humans.

Glycerol kinetics were evaluated during high-intensity exercise in five untrained and five endurance-trained subjects. Glycerol rate of appearance (Ra) in plasma was determined by infusing [2H5]glycerol during rest and 60 minutes of cycle ergometer exercise performed at 70% V02 peak. Mean plasma glycerol concentration was greater in trained than untrained subjects throughout exercise (P<.05). The average glycerol Ra during exercise and the integrated lipolytic response to exercise, expressed as total glycerol Ra above baseline, were both greater in trained (7.85 +/- 0.72 micromol x kg(-1) x min(-1) and 289 +/- 50 micromol x kg(-1) x h(-1), respectively) than in untrained (5.68 +/- 0.90 micromol x kg(-1) x min(-1), and 198 +/- 31 micromol x kg(-1) x h(-1), respectively) subjects (P<.05). We conclude that whole-body lipolytic rates are greater in endurance-trained athletes than in sedentary controls during high-intensity exercise performed at the same relative intensity.

Adult

An animal model for measurement of protein metabolism in the skin.

BACKGROUND: A suitable in vivo approach with which to quantify skin protein metabolism has not been found, and consequently no information exists relating protein synthesis to protein breakdown in the fasted state. METHODS: Stable isotope-labeled phenylalanine was infused into five fasted rabbits, and amino acid and protein kinetics were calculated from a three-compartment model with the rabbit ear used as an arteriovenous balance mode. Results were compared with the more traditional but limited direct incorporation technique to measure synthesis. RESULTS: The model-derived skin protein synthesis rate was 0.34%/hr +/- 0.04%/hr, which was almost identical to the value of 0.30%/hr +/- 0.01%/hr determined by the direct incorporation method. The model-derived skin protein breakdown rate was only slightly higher than the synthesis rate, meaning protein balance was generally maintained in the fasted state because of the efficient reuse of amino acids from protein breakdown. CONCLUSIONS: The newly described rabbit ear model is a reliable approach to the determination of the amino acid and protein kinetics in the skin in vivo. Efficient reuse of amino acids released from proteolysis explains the maintenance of skin integrity during brief fasting.

Animals

Beta-blockade lowers peripheral lipolysis in burn patients receiving growth hormone. Rate of hepatic very low density lipoprotein triglyceride secretion remains unchanged.

OBJECTIVE: The purpose of this study was to determine the effect of propranolol on peripheral lipolysis in massively burned children during treatment with recombinant human growth hormone (rhGH), and to ascertain whether decreased free fatty acid availability for re-esterification would alter the hepatic rate of secretion of triglycerides (TGs) bound to very low density lipoproteins (VLDLs). BACKGROUND: Fatty liver occurs in severely burned patients, often resulting in a twofold increase in liver size. This could be the result of an imbalance between increased provision of free fatty acids from peripheral lipolysis, coupled with no increase in fat oxidation, and insufficient rate of secretion of TGs from the liver. METHODS: In a cross-over study, six burned children were treated with either rhGH or rhGH plus propranolol. On the sixth day of treatment, isotopic tracer infusions were conducted to determine the rate of release of free fatty acid (Ra FFA) from peripheral tissue and the rate of secretion of VLDL-bound TGs by the liver. RESULTS: Exogenous rhGH increased Ra FFA in children with large third-degree burns. Propranolol decreased Ra FFA, but the rate of secretion of fatty acids in the form of VLDL-TG from the liver was maintained. Plasma FFA, as opposed to fatty acids newly synthesized in the liver, were the primary precursors for hepatic triglyceride synthesis. CONCLUSIONS: The administration of propranolol to burned children receiving rhGH is safe, has salutary cardiovascular effects, decreases the release of FFA from adipose tissue and increases the efficiency of the liver in secreting fatty acids as VLDL TGs.

Adolescent

Pyruvate dehydrogenase inactivity is not responsible for sepsis-induced insulin resistance.

OBJECTIVE: To determine whether activation of pyruvate dehydrogenase with dichloroacetate can reverse sepsis-induced insulin resistance in humans or rats. DESIGN: Prospective, controlled study. SETTING: Intensive care unit (ICU) and laboratory at a university medical center. SUBJECTS: Nine patients were admitted to the ICU with Gram-negative sepsis, confirmed by cultures. In addition, chronically instrumented, Sprague-Dawley rats, either controls or with live Escherichia coli-induced sepsis. INTERVENTIONS: Hyperinsulinemic euglycemic clamp, with or without coadministration of dichloroacetate. MEASUREMENTS AND MAIN RESULTS: In humans, a primed, constant infusion of [6,6-2H2]glucose was used to determine endogenous glucose production and whole-body glucose disposal. Septic humans exhibited impaired maximal insulin-stimulated glucose utilization (39.5 +/- 2.7 mumol/kg/min), despite complete suppression of endogenous glucose production. In rats, a primed, constant infusion of [3-3H]glucose was used to determine endogenous glucose production and whole-body glucose disposal. Tissue glucose uptake in vivo was determined by [14C]-2-deoxyglucose uptake. Maximal, whole-body, insulin-stimulated glucose utilization was 205 +/- 11 and 146 +/- 9 mumol/kg/min in control and septic rats, respectively. The defect was specific to skeletal muscle and heart. Stimulation of pyruvate dehydrogenase with dichloroacetate caused a 50% decrease in plasma lactate concentration but failed to improve whole-body insulin-stimulated glucose utilization in either the septic human or rat. Dichloroacetate reversed the impairment of insulin-stimulated myocardial glucose uptake in septic rats, but did not influence skeletal muscle glucose uptake either under basal conditions or during insulin stimulation. CONCLUSIONS: Activation of pyruvate dehydrogenase with dichloroacetate does not ameliorate the impairment of whole-body, insulin-stimulated glucose uptake in septic humans or rats, or reverse the specific defect in insulin-mediated skeletal muscle glucose uptake by septic rats. Therefore, the decreased pyruvate dehydrogenase activity associated with sepsis does not appear to mediate sepsis-induced insulin resistance during insulin-stimulated glucose uptake at either the whole-body or tissue level.

APACHE

Regulation of the insulin-like growth factor system by insulin in burn patients.

The aim of the present investigation was to determine whether there is a net uptake of insulin-like growth factor I (IGF-I) or IGF-binding proteins (IGFBPs) by the leg after burn injury and to elucidate the regulatory role of insulin exerted on this system under in vivo conditions in burn patients. Studies were performed on nine patients after burn injury (approximately 60% body surface area). Each patient was studied twice during a continuous infusion of a carbohydrate-rich enteral diet. Blood was collected simultaneously from the femoral artery and vein for the measurement of various elements of the IGF system after 7 days of enteral diet alone (basal period) and after 7 days of the enteral diet plus the infusion of insulin (insulin period). Data from these patients were compared to values in age-matched fed healthy volunteers. During the basal period, burn patients demonstrated a significant reduction in the venous concentration of IGF-I and an increase in both IGFBP-1 and -2 compared to control values. Insulin produced a significant 15% increase in the IGF-I concentration in burn patients, but decreased the circulating levels of IGFBP-1 by 50%. The IGF-I and IGFBP-1 concentrations at the end of the insulin period were still significantly different from those in control subjects. Burn patients also exhibited a marked reduction in intact IGFBP-3 and the acid-labile subunit under basal conditions, and these alterations were not reversed by insulin. Under basal conditions, all burn patients had a positive arterio-venous (A-V) difference for IGF-I across the leg. The A-V difference was increased 50% in response to insulin. The net uptake of IGF-I by the leg was 2.4 micrograms/min under basal conditions, and as leg blood flow also tended to increase in response to insulin, IGF-I uptake was elevated more than 3-fold during the insulin period. No A-V difference across the leg was detected for IGFBP-1, -2, or -3 in burn patients. In conclusion, burn injury in humans produces dramatic and sustained alterations in various components of the IGF system that persist despite adequate nutritional support. Our data indicate the presence of a net uptake of IGF-I by the leg in burn patients that may serve to counteract the catabolic state.

Adolescent

Role of membrane transport in interorgan amino acid flow between muscle and small intestine.

In the fasting state, amino acids are released from the periphery to be used in splanchnic tissues. To understand the mechanism of such interorgan substrate exchange at the tissue level, we have determined the relationships between inward and outward amino acid transport and intracellular amino acid kinetics in the small intestine and skeletal muscle of postabsorptive anesthetized dogs. In the gut, amino acids appearing intracellularly (from inward transport, protein degradation, and absorption from the lumen) were used for protein synthesis more efficiently (P < .05) than in muscle (phenylalanine, 55% +/- 5% v 13% +/- 3%; lysine, 70% +/- 7% v 28% +/- 3%). In contrast, in muscle, amino acids appearing intracellularly (from inward transport and protein degradation) were preferentially (P < .05) released into the bloodstream, as opposed to being incorporated into protein (phenylalanine, 87% +/- 4%; lysine, 72% +/- 3%). Inward transport accounted for a greater (P < .05) proportion of total intracellular amino acid appearance in the gut than in muscle (leucine, 63% +/- 3% v 37 +/- 3%; valine, 75% +/- 5% v 53% +/- 3%; phenylalanine, 66% +/- 1% v 50% +/- 4%; lysine, 52% +/- 2% v 31% +/- 2%). We conclude that differences in transmembrane amino acid transport kinetics in both the inward and outward directions contribute to the net flow of amino acids from the muscle to the gut in the fasting state.

Amino Acids

Total energy expenditure during total parenteral nutrition: ambulatory patients at home versus patients with sepsis in surgical intensive care.

BACKGROUND: To avoid the complications associated with overfeeding or underfeeding, the energy requirements of patients receiving total parenteral nutrition (TPN) must be accurately prescribed. However, until recently it has not been possible to directly measure the rates of total energy expenditure (TEE) in surgical patients receiving TPN. METHODS: Values for total body water and TEE in four patients with sepsis (mean Acute Physiology and Chronic Health Evaluation [APACHE] score, 10) receiving TPN in surgical intensive care unit and in four patients with chronic intestinal failure receiving long-term TPN at home (HPN) have been determined by using the doubly labeled water technique. The values for TEE have been compared with those of resting energy expenditure obtained with indirect calorimetry (REE CAL) and calculated by using the Harris-Benedict equation (REE HB). RESULTS: In both the patients with sepsis and the patients receiving HPN the proportion of body weight made up of water was normal for patient age and gender. In patients with sepsis the REE HB significantly (p < 0.05) underestimated the REE CAL (15.39 +/- 3.80 kcal/kg/day-1 versus 31.3 +/- 1.23 kcal/kg/day-1) and was significantly less than the TEE derived by using doubly labeled water (44.62 +/- 1.09 kcal/kg/day-1; p < 0.001). In the ambulatory patients receiving HPN no difference was noted between the REE HB and the REE CAL (18.02 +/- 0.41 kcal/kg/day-1 versus 21.37 +/- 0.94 kcal/kg/day-1). The average TEE for these patients was 30.25 +/- 3.42 kcal/kg/day-1, and this was significantly greater (p < 0.006) than both REE CAL and REE HB: CONCLUSIONS: This investigation has shown that in patients with sepsis TEE constitutes 1.4 times the REE CAL or approximately 40 kcal/kg/day, whereas in HPN patients TEE can be estimated by supplying 1.4 times the REE or approximately 30 kcal/kg/day-1.

Adult

Insulin-like growth factor-I and insulin reduce leucine flux and oxidation in conscious tumor necrosis factor-infused dogs.

BACKGROUND: We have tested the hypothesis that insulin-like growth factor-I (IGF-I) or insulin can prevent the protein catabolic effects of tumor necrosis factor (TNF). METHODS: After a 2-hour basal period TNF was infused (prime, 2.5 micrograms.kg-1; constant, 31.25 ng.kg-1.min-1) for 4 hours into conscious dogs to create the catabolic state. After 2 hours of TNF infusion either recombinant human IGF-I (n = 5) or recombinant human insulin (n = 5) was infused for an additional 2 hours. A third group (n = 5) received TNF alone for 4 hours. RESULTS: TNF infusion caused an increase in both glucose production, reflected by [6,6-d2]glucose tracer data, and net protein catabolism, reflected by both [1-13C]leucine and [15N2]urea tracer methods. IGF-I and insulin both significantly reduced the rates of appearance of leucine and leucine oxidation to a similar extent, resulting in the significant decrease in net protein catabolism. CONCLUSIONS: IGF-I and insulin can ameliorate the catabolic effects of TNF on protein and glucose metabolism equally effectively, although more IGF-I is required on a molar basis.

Animals

Stimulation of muscle protein synthesis by long-term insulin infusion in severely burned patients.

OBJECTIVE: To determine if long-term (7 days) infusion of insulin can ameliorate altered protein kinetics in skeletal muscle of severely burned patients and to investigate the hypothesis that changes in protein kinetics during insulin infusion are associated with an increased rate of transmembrane amino acid transport from plasma into the intracellular free amino acid pool. SUMMARY BACKGROUND DATA: In critically ill patients, vigorous nutritional support alone may often fail to entirely curtail muscle catabolism; insulin stimulates muscle protein synthesis in normal volunteers. METHODS: Nine patients with severe burns were studied once during enteral feeding alone (control period), and once after 7 days of high-dose insulin. The order of treatment with insulin was randomized. Data were derived from a model based on a primed-continuous infusion of L-[15N]phenylalanine, sampling of blood from the femoral artery and vein, and biopsies of the vastus lateralis muscle. RESULTS: Net leg muscle protein balance was significantly (p < 0.05) negative during the control period. Exogenous insulin eliminated this negative balance by stimulating protein synthesis approximately 350% (p < 0.01). This was made possible in part by a sixfold increase in the inward transport of amino acids from blood (p < 0.01). There was also a significant increase in leg muscle protein breakdown. The new rates of synthesis, breakdown, and inward transport during insulin were in balance, such that there was no difference in the intracellular phenylalanine concentration from the control period. The fractional synthetic rate of protein in the wound was also stimulated by insulin by approximately 50%, but the response was variable and did not reach significance. CONCLUSIONS: Exogenous insulin may be useful in promoting muscle protein synthesis in severely catabolic patients.

Adolescent

Increased plasma glucose clearance in sepsis is due to increased exchange between plasma and interstitial fluid.

It has long been unclear why plasma glucose clearance is increased during sepsis, an insulin-resistant state. To address this issue, we studied sheep given a constant infusion of endotoxin for at least 24 h (n = 5). We gave a bolus of 6,6 d2 glucose and determined the fractional exchange of glucose between plasma and interstitial fluid using compartmental modeling techniques. We found that exchange of glucose between plasma and interstitial fluid was significantly increased in sepsis, but the fractional clearance of glucose from interstitial fluid was not significantly altered. Thus the observed increased plasma glucose clearance was solely due to alterations in glucose exchange between plasma and interstitial fluid and was unrelated to glucose transport into cells.

Animals

Transmembrane transport and intracellular kinetics of amino acids in human skeletal muscle.

We have used stable isotopic tracers of amino acids to measure in vivo transmembrane transport of phenylalanine, leucine, lysine, alanine, and glutamine as well as the rates of intracellular amino acid appearance from proteolysis, de novo synthesis, and disappearance to protein synthesis in human skeletal muscle. Calculations were based on data obtained by the arteriovenous catheterization of the femoral vessels and muscle biopsy. We found that the fractional contribution of transport from the bloodstream to the total intracellular amino acid appearance depends on the individual amino acid, varying between 0.63 +/- 0.02 for phenylalanine and 0.22 +/- 0.02 for alanine. Rates of alanine and glutamine de novo synthesis were approximately eight and five times their rate of appearance from protein breakdown, respectively. The model-derived rate of protein synthesis was highly correlated with the same value calculated by means of the tracer incorporation technique. Furthermore, amino acid transport rates were in the range expected from literature values. Consequently, we conclude that our new model provides a valid means of quantifying the important aspects of protein synthesis, breakdown, and amino acid transport in human subjects.

Adult

Increased rates of muscle protein turnover and amino acid transport after resistance exercise in humans.

The rates of protein synthesis and degradation and of amino acid transport were determined in the leg muscle of untrained postabsorptive normal volunteers at rest and approximately 3 h after a resistance exercise routine. The methodology involved use of stable isotopic tracers of amino acids, arteriovenous catheterization of the femoral vessels, and biopsy of the vastus lateralis muscle. During postexercise recovery, the rate of intramuscular phenylalanine utilization for protein synthesis increased above the basal value by 108 +/- 18%, whereas the rate of release from proteolysis increased by 51 +/- 17%. Muscle protein balance improved (P < 0.05) after exercise but did not become positive (from -15 +/- 12 to -6 +/- 3 nmol phenylalanine.min-1.100 ml leg volume-1). After exercise, rates of inward transport of leucine, lysine, and alanine increased (P < 0.05) above the basal state from 132 +/- 16 to 208 +/- 29, from 122 +/- 8 to 260 +/- 8, and from 384 +/- 71 to 602 +/- 89 nmol.min-1.100 ml leg-1, respectively. Transport of phenylalanine did not change significantly. These results indicate that, during recovery after resistance exercise, muscle protein turnover is increased because of an acceleration of synthesis and degradation. A postexercise acceleration of amino acid transport may contribute to the relatively greater stimulation of protein synthesis.

Adult

Quantification of incorporation of [15N]ammonia into plasma amino acids and urea.

The incorporation of 15N into individual plasma amino acids and urea was quantified in five human subjects who received 15NH4Cl either orally or intravenously for 6 h. After oral tracer administration, the highest enrichment was achieved by arginine, followed by urea and glutamine; distribution of 15N within glutamine was 55% amide and 45% amino N. Glutamine achieved the highest enrichment after the intravenous administration of tracer, with a distribution of 92% amide and 8% amino N. The relative distribution pattern of 15N incorporation was quantified from the rate at which 15N initially appeared in each plasma component. Amino acids (especially arginine, glutamine, and glutamate) accounted for greater than one-half (54%) of the orally administered tracer that was initially recovered in plasma components, compared with 46% initial appearance for urea; for the intravenous tracer, amino acids accounted for 78% of initial appearance of tracer compared with 22% for urea. Our results highlight the involvement of the splanchnic bed in the utilization of orally administered ammonia (preferential incorporation of oral tracer into arginine, urea, glutamate, and the amino N of glutamine) in contrast to the preferential incorporation of systemically administered ammonia into the amide N of glutamine and alanine.

Administration, Oral

A new correction factor for use in tracer estimations of plasma fatty acid oxidation.

The purpose of this study was to acquire a new correction factor for use in tracer estimations of plasma fatty acid oxidation that would fully account for label fixation during the infusion of fatty acid tracers. Thus volunteers were infused with 13C-labeled fatty acids and [1-14C]acetate in the basal state, during hyperinsulinemia-hyperglycemia (clamp), and during 1 h of cycling exercise. The fractional recovery of acetate label (i.e., the acetate correction factor) was 0.56 +/- 0.02, 0.50 +/- 0.03, and 0.80 +/- 0.03 in the basal state and during the clamp and exercise, respectively. Isotopically determined plasma fatty acid oxidation rates (mumol.kg-1.min-1) were 1.7 +/- 0.2, 0.8 +/- 0.2, and 6.4 +/- 0.5 (no correction); 2.1 +/- 0.2, 1.0 +/- 0.2, and 6.7 +/- 0.5 (bicarbonate correction); and 3.1 +/- 0.2, 1.5 +/- 0.2, and 8.2 +/- 0.4 (acetate correction). We conclude that use of the acetate correction factor in place of the bicarbonate correction factor should improve the accuracy of isotopic measurements of plasma fatty acid oxidation, because it accounts for label fixation that might occur at any step between the entrance of labeled acetyl-CoA into the tricarboxylic acid cycle until the recovery of label in breath CO2.

Acetates

Testosterone administration to elderly men increases skeletal muscle strength and protein synthesis.

Aging men develop a significant loss of muscle strength that occurs in conjunction with a decline in serum testosterone concentrations. We investigated the effects of testosterone administration to six healthy men [67 +/- 2 (SE) yr] on skeletal muscle protein synthesis, strength, and the intramuscular insulin-like growth factor I (IGF-I) system. Elderly men with serum testosterone concentrations of 480 ng/dl or less were given testosterone injections for 4 wk to produce serum concentrations equal to those of younger men. During testosterone administration muscle strength (isokinetic dynamometer) increased in both right and left hamstring and quadricep muscles as did the fractional synthetic rate of muscle protein (stable-isotope infusion). Ribonuclease protection assays done on total RNA from muscle showed that testosterone administration increased mRNA concentrations of IGF-I and decreased mRNA concentrations of insulin-like growth factor binding protein-4. We conclude that increasing testosterone concentrations in elderly men increases skeletal muscle protein synthesis and strength. This increase may be mediated by stimulation of the intramuscular IGF-I system.

Aged

Isotopic determination of glycolytic flux during intense exercise in humans.

We used a new stable isotope tracer approach incorporating muscle intracellular lactate enrichment to determine the flux of glucose/glucosyl toward lactate [i.e., nonoxidized pyruvate (Pyr) production (Pyrno)] in moderately trained cyclists exercising at approximately 80% (259 +/- 16 W; n = 6) and approximately 100% (341 +/- 9 W; n = 8) maximal O2 uptake (VO2max). Primed constant infusions of [6,6-2H2]glucose and [13C]lactate or [13C]Pyr tracers were given, and rapid achievement of plateau was obtained during exercise by increasing the infusion rates at exercise onset to correspond with expected increases in production. The accumulated O2 deficit was simultaneously determined over the 1st 3 min of exercise as an indirect means of quantifying glycolytic flux for comparison with our tracer-determined values and was significantly greater at the higher intensity (38 +/- 3 vs. 30 +/- 3 ml O2.kg-1.3 min-1; P < 0.02). Pyrno was also significantly higher (6.38 +/- 0.91 vs. 4.38 +/- 0.65 mmol.kg-1.min-1 over 3 min at 100 and 80% VO2max, respectively). The blood lactate rate of appearance at approximately 100% VO2max (828 +/- 69 mumol.kg-1.min-1) represented a higher percentage of Pyr rate of appearance (RaPyr; 31 +/- 3%) than that at approximately 80% VO2max (416 +/- 36 mumol.kg-1.min-1; 22 +/- 2%; P < 0.02). Although only approximately 27 +/- 2% of RaPyr was oxidized, this provided 78 +/- 2% of the total energy demand during the 1st 3 min of exercise at either intensity. Our new method provided values for Pyrno that were in the expected range and were highly correlated with respective accumulated O2 deficit values (r = 0.87, P < 0.0001). In conclusion, our new tracer method appears to be valid for the measurement of RaPyr and Pyrno during high-intensity exercise lasting even < 10 min.

Adult

Effect of exercise on lipolytic sensitivity in endurance-trained athletes.

Studies performed in vitro suggest that an acute bout of exercise increases the lipolytic response to beta-adrenergic stimulation. We evaluated the effect of exercise on lipolytic sensitivity in vivo in five endurance-trained athletes. The rate of appearance (Ra) of glycerol in plasma, an index of whole body lipolysis, was determined during 60 min of epinephrine infusion (0.015 microgram.kg-1.min-1) on two occasions: 1) at basal resting conditions and 2) 90 min after completing 1 h of high-intensity (70% O2 uptake) cycle ergometer exercise. Total glycerol Ra during epinephrine infusion in the basal state (352 +/- 35 mumol.kg-1. 60 min-1) was not significantly different from the value obtained after high-intensity exercise (439 +/- 58 mumol.kg-1. 60 min-1). However, the increase in glycerol Ra above baseline during epinephrine infusion was lower after (30 +/- 16 mumol.kg-1. 60 min-1) than before (148 +/- 28 mumol.kg-1. 60 min-1) exercise because of the high postexercise baseline value (P < 0.05). Mean plasma free fatty acid (FFA) concentration was lower during exercise than during epinephrine infusion despite a greater rate of lipolysis during exercise. The slope of change in plasma FFA with respect to glycerol RA was lower during exercise (0.0171 +/- 0.006) than during epinephrine infusion (0.0835 +/- 0.018) (P < 0.05). We conclude that a single bout of intense exercise does not increase in vivo lipolytic sensitivity to beta-adrenergic stimulation in endurance-trained athletes. In addition, plasma FFA concentration represents the balance between plasma FFA inflow and tissue uptake and cannot be used as an index of lipolytic activity during certain physiological conditions, such as exercise.

Adult