Biomedical subjects

K R Feingold

Publications and source records attributed to K R Feingold.

At least 145 records · Page 8Linked to original sources

PubMed1995

Discordant regulation of proteins of cholesterol metabolism during the acute phase response.

Recent studies have shown that the administration of endotoxin (LPS) and cytokines to Syrian hamsters increases serum cholesterol levels, hepatic cholesterol synthesis, and the activity, protein levels, and mRNA levels of hepatic HMG-CoA reductase. Despite the greater than 10-fold increase in HMG-CoA reductase mRNA levels, LPS had only minimal effects on hepatic LDL receptor mRNA levels. In the present study, we demonstrate that LPS increases the transcription rate in the liver of HMG-CoA reductase mRNA approximately 4- to 5-fold without affecting LDL receptor mRNA transcription. Most stimuli that regulate HMG-CoA reductase and LDL receptor mRNA levels also regulate, in parallel, HMG-CoA synthase and farnesyl pyrophosphate (FPP) synthetase. However, in chow-fed animals, LPS and cytokines (TNF, IL-1, TNF + IL-1) increased hepatic HMG-CoA reductase mRNA levels without increasing LDL receptor, HMG-CoA synthase, or FPP synthetase mRNA levels. The feeding of cholesterol or bile resin binders regulates the mRNA levels of HMG-CoA reductase, LDL receptor, HMG-CoA synthase, and FPP synthetase. In both cholesterol- and colestipol-fed animals, LPS increased HMG-CoA reductase mRNA levels while either decreasing or causing minimal increases in the mRNA levels of the other proteins.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute-Phase Reaction↗

PubMed1995

Endotoxin and TNF lead to reduced plasma LCAT activity and decreased hepatic LCAT mRNA levels in Syrian hamsters.

Endotoxin (LPS) administration, which mimics infection, stimulates the production of many cytokines, including TNF, that are thought to mediate the alterations in lipid metabolism that occur during infection. The aims of this study were to determine the effect of LPS or TNF administration on plasma LCAT activity and hepatic LCAT mRNA levels in Syrian hamsters. Plasma LCAT activity was decreased 8 h after LPS administration, reached a maximum level of inhibition at 16 h which persisted for at least 24 h, at which time the activity was 53% of control values. The decrease in plasma LCAT activity was first seen at an LPS dose of 0.01 microgram/100 g body weight and reached a maximum at 50-100 micrograms/100 g body weight. The ratio of free to esterified cholesterol in the plasma increased in the LPS-treated animals. Moreover, LPS administration decreased LCAT mRNA levels in the liver. The decrease in hepatic LCAT mRNA levels preceded the decrease in plasma LCAT activity. Additionally, TNF treatment (16.7 micrograms/100 g body weight) decreased plasma LCAT activity by 35% and LCAT mRNA levels in the liver by 60% 16 h after administration. Lastly, in cultured rat H35 hepatocytes, TNF decreased LCAT mRNA levels in the liver by 60% 16 h after administration. Lastly, in cultured rat H35 hepatocytes, TNF decreased LCAT mRNA levels by 50% with a 1/2 maximal dose of approximately 1 ng/ml. Thus, plasma LCAT activity and hepatic mRNA levels are decreased by LPS or TNF treatment. LCAT is a member of a group of proteins that affect lipid and lipoprotein metabolism whose levels are altered during the host's acute phase response.

Animals↗

PubMed1995

Extracellular processing of phospholipids is required for permeability barrier homeostasis.

Three key lipid types, cholesterol, ceramides (CER), and free fatty acids (FA), form the stratum corneum (SC) lamellar bilayers that mediate barrier function. Prior studies have shown that barrier requirements regulate CER generation from glucosylCER, and that this catabolic step takes place within the SC interstices. Here, we addressed whether extracellular processing of phospholipids (PL), the FA precursor delivered to the SC interstices with glucosylCER and cholesterol during exocytosis of lamellar body contents, is also required for barrier homeostasis. We applied two chemically unrelated inhibitors of phospholipase A2 (PLA2-I), BPB (irreversible) and MJ33 (reversible), topically to hairless mice after barrier perturbation with acetone. Both inhibitors delayed barrier recovery at non-cytotoxic doses, while MJ45, an analogue known to inhibit PLA2-II but not PLA2-I, had no effect. Moreover, the delays in barrier recovery induced by BPB and MJ33 could be overridden by co-applications of palmitic acid, but not linoleic acid or lysolecithin. Furthermore, inhibitor-treatment resulted in accumulation of PL and depletion of FA in the SC by 4 h, as well as the persistence of "immature" lamellar body-derived membrane structures in the SC interstices. Finally, these changes in membrane structure were reversed when inhibitor-treated SC was incubated in vitro with palmitic acid. These studies show that: 1) inhibition of PLA2 results in abnormalities in lipid composition and SC structure that alter barrier homeostasis; and 2) the functional defect can be attributed to a deficiency of nonessential FA within the SC. Thus, extracellular processing of PL into FA is required for normal barrier function.

Animals↗

PubMed1995

Lipoteichoic acid stimulates lipolysis and hepatic triglyceride secretion in rats in vivo.

The host response to infection is frequently accompanied by changes in lipid metabolism. Previous studies have shown that endotoxin (LPS), a component of the cell wall of gram-negative bacteria, increases serum lipid levels. In this study, we demonstrate that lipoteichoic acid (LTA), a component of the cell membrane of gram-positive bacteria, also increases serum lipid levels in rats in a dose-dependent manner (0.1-300 micrograms/200 g body weight). Serum triglyceride levels increased within 2 h after LTA administration with peak values at 4 h (2-fold increase). Serum cholesterol levels also increased but the effect was delayed occurring at 16 h and was relatively small (1.2-fold increase). LTA (10 micrograms/200 g BW) did not decrease adipose tissue lipoprotein lipase activity or the clearance of triglyceride-rich lipoproteins. Rather, the LTA-induced hypertriglyceridemia is due to an increase in hepatic triglyceride secretion. LTA stimulates both hepatic de novo fatty acid synthesis and lipolysis. The increased delivery of free fatty acids to the liver plays a major role in the LTA-induced hypertriglyceridemia. Pretreatment with phentolamine, an alpha-adrenergic receptor antagonist, and alprenolol, a beta-adrenergic receptor antagonist, or phentolamine alone significantly suppressed the hypertriglyceridemia induced by LTA. These adrenergic inhibitors had no significant effect on the increase in lipolysis. These results indicate that catecholamines are involved in mediating the LTA-induced increase in hepatic triglyceride secretion via alpha-adrenergic receptors. These changes in lipid metabolism may play an important role in the organism's response to gram-positive infection.

Adipose Tissue↗

PubMed1994

Permeability barrier disruption alters the localization and expression of TNF alpha/protein in the epidermis.

Previous studies have shown that (1) epidermal TNF alpha mRNA levels are increased following acute disruption of the cutaneous permeability barrier; (2) this increase is maximal at 1 h and decreases to control levels by 8 h; and (3) in essential fatty acid-deficient (EFAD) mice, a chronic model of barrier perturbation, TNF alpha mRNA levels are also elevated several-fold over controls. In the present study we determined, using immunocytochemical procedures, epidermal TNF alpha protein levels following either acute of chronic barrier disruption and the localization of any increase. Frozen, paraffin and Antibed sections of skin were incubated with polyclonal anti-mouse TNF alpha antisera and detection was accomplished by either immunoperoxidase or fluorescence procedures. We found that (1) TNF alpha-immunoreactive protein was present in normal mouse epidermis, and was primarily localized to the upper nucleated layers where it displayed a diffuse cytosolic pattern; (2) acute disruption of the barrier with acetone or tape-stripping resulted in TNF alpha staining that was more intense throughout all of the nucleated epidermal cell layers in comparison with normal epidermis; (3) the increase in TNF alpha staining occurred as early as 2 h after barrier disruption; and (4) increased TNF alpha staining was also observed in the stratum corneum of EFAD mice. These results indicate that epidermal TNF alpha protein levels increase after both acute and chronic barrier disruption, and are consistent with the hypothesis that TNF alpha may signal and/or coordinate portions of the cutaneous response to barrier disruption.

Animals↗

PubMed1994

Diabetes increases hepatic hydroxymethyl glutaryl coenzyme A reductase protein and mRNA levels in the small intestine.

Previous studies have shown that both cholesterol synthesis and the activity of hepatic hydroxymethyl glutaryl coenzyme A (HMG CoA) reductase, the rate-limiting enzyme in cholesterol synthesis, are increased in the small intestine of a wide variety of different animal models of diabetes. In the present study, we demonstrate that the mass of HMG CoA reductase protein is increased in the small intestine of both streptozocin-induced diabetic rats (2.5-fold) and streptozocin/alloxan-induced diabetic dogs (2.4-fold). These increases in HMG CoA reductase protein mass are of a magnitude similar to the previously observed increases in either HMG CoA reductase activity and/or cholesterol synthesis in the small intestine of diabetic animals. Furthermore, mRNA levels for HMG CoA reductase in the small intestine of diabetic rats and diabetic dogs are increased 2.1- and 1.7-fold, respectively. These results suggest that the increase in HMG CoA reductase protein levels in the small intestine of diabetic animals is due to an increase in mRNA levels. In contrast, mRNA levels for HMG CoA reductase in the liver of diabetic rats are not increased. Additionally, mRNA levels for the low-density lipoprotein (LDL) receptor are also increased in the small intestine of diabetic animals (rats, 43%; dogs, 59%). The increase in small-intestinal cholesterol synthesis has the potential for adversely affecting lipoprotein metabolism and increasing the risk of atherosclerosis in diabetes.

Animals↗

PubMed1994

Cytokines induce catabolic effects in cultured adipocytes by multiple mechanisms.

Previous studies have demonstrated that some cytokines induce a coordinate catabolic response in adipose cells which leads to decreased fat storage. The mechanisms by which cytokines cause these effects are unknown. The primary purpose of the present study was to determine the effects of TNF, IL-1, IFN-alpha and IFN-alpha on the mRNA levels of the key enzymes involved in fat metabolism in 3T3-F442A adipocytes. TNF, IL-1, IFN-alpha and IFN-gamma decreased lipoprotein lipase activity and increased lipolysis in adipocytes. TNF, IFN-alpha and IFN-gamma decreased fatty acid synthesis while IL-1 increased fatty acid synthesis. However, the cytokine effects on mRNA levels were not always consistent with the observed changes in activity and were unique for each cytokine. Specifically, while all cytokines decreased LPL activity, only TNF and IFN-gamma decreased LPL mRNA levels. In addition, while TNF, IFN-alpha and IFN-gamma decreased fatty acid synthesis, only TNF significantly decreased the mRNA levels of both acetyl CoA carboxylase and fatty acid synthase, the key enzymes in fatty acid synthesis. IFN-alpha and IFN-gamma decreased fatty acid synthase mRNA levels without significantly altering acetyl CoA carboxylase mRNA. IL-1 caused a slight increase in fatty acid synthesis and increased acetyl CoA carboxylase mRNA levels. Finally, while all cytokines increased lipolysis, hormone sensitive lipase mRNA levels were decreased by TNF, IFN-alpha and IFN-gamma treatment. These results indicate that the regulation of adipocyte lipid metabolism by cytokines is complex and that coordinate changes in mRNA levels cannot account for the observed metabolic changes.(ABSTRACT TRUNCATED AT 250 WORDS)

3T3 Cells↗

PubMed1994

Fatty acid synthesis in obese insulin resistant diabetic mice.

Diabetes is associated with hypertriglyceridemia and it has been suggested that the intestine contributes to this elevation. Recent studies have shown that in animals with IDDM, fatty acid (FA) synthesis is decreased in the liver and increased in the small intestine (SI). The purpose of the present study was to measure FA synthesis in the liver and SI of animals with NIDDM. In both db/db and ob/ob animals the incorporation of 3H2O into FA was increased in the SI (10 fold in db/db and 2.2 fold in ob/ob). FA synthesis was also increased in the liver of NIDDM (9 fold in db/db and 6 fold in ob/ob). These results provide further evidence that diabetes leads to changes in lipid metabolism in the SI.

Animals↗

PubMed1994

Effects of endotoxin and cytokines on lipid metabolism.

Endotoxin, via cytokines, induces marked changes in lipid metabolism: serum VLDL increases, whereas the effect on LDL levels varies among species. The increase in VLDL is caused by stimulation of hepatic VLDL secretion or inhibition of clearance, or both. These alterations can be deleterious or beneficial effects.

Animals↗

PubMed1994

Selective obliteration of the epidermal calcium gradient leads to enhanced lamellar body secretion.

The epidermal permeability barrier is formed by lipids delivered to the intercellular spaces through the secretion of lamellar bodies. Prior studies have shown that the rate of lamellar body secretion appears to be regulated by the extracellular calcium content of the upper epidermis, which is altered following permeability barrier disruption. To determine directly whether changes in extracellular calcium content in the upper epidermis versus disruption of the barrier regulate lamellar body secretion, we experimentally manipulated the Ca++ content of the upper epidermis by sonophoresis of aqueous solutions containing physiologic Ca++ (and K+) versus ion-free solutions across hairless mouse stratum corneum. Sonophoresis at 15 MHz did not alter barrier function, but in the absence of Ca++ the extracellular calcium content of the outer epidermis, as revealed by ion capture cytochemistry, was displaced downward toward the basal layer and dermis. In contrast, following sonophoresis of Ca(++)-containing solutions, the extracellular Ca++ gradient became obscured by excess Ca++ in the cytosol at all levels of the epidermis. These changes in the extracellular calcium content lead, in turn, to accelerated lamellar body secretion (with low Ca++), or basal rates of lamellar body secretion (with normal Ca++). These results demonstrate that the epidermal extracellular calcium content in the upper epidermis can be manipulated by sonophoresis without prior barrier disruption, and that changes in the Ca++ gradient induce lamellar body secretion, independent of barrier disruption.

Animals↗

PubMed1994

Influence of altered serum cholesterol levels and fasting on cutaneous cholesterol synthesis.

Barrier perturbation stimulates epidermal cholesterol synthesis, which plays an important role in restoring barrier function. In the present study, we examined whether changes in serum cholesterol levels or nutrition regulate epidermal cholesterol synthesis in hairless mice. Serum cholesterol levels were lowered by 50% after injection with 4-aminopyrazolo (3,4-d) pyrimidine and were increased by 51% by feeding an atherogenic diet. In contrast to most other tissues, cholesterol synthesis in the epidermis and dermis was not inhibited by elevations or stimulated by decreases in serum cholesterol levels. Additionally, feeding a high-cholesterol diet did not decrease epidermal or dermal cholesterol synthesis. However, fasting significantly decreased both epidermal (38%) and dermal (34%) cholesterologenesis. Furthermore, barrier recovery after acetone disruption of the barrier was impaired in fasted animals. However, treatment with topical lipids did not restore barrier repair rate to normal, indicating that factors in addition to lipids are necessary to overcome the effects of fasting. These results demonstrate that cholesterol synthesis in the epidermis and dermis is regulated independently of changes in serum cholesterol levels.

Adenine↗

PubMed1994

A role for ions in barrier recovery after acute perturbation.

The epidermal cutaneous permeability barrier can be disrupted by treatment with topical solvents. Recent studies have shown that barrier recovery, measured by the recovery of transepidermal water loss towards normal, is inhibited by high extracellular Ca++ and K+, and accelerated by low extracellular concentrations of these ions. To examine the effects of Ca++ or K+ fluxes on barrier recovery, we tested the effects on transepidermal water loss recovery of agents that modify these fluxes. K+ channel agonists or blockers modified the inhibitory effects on barrier recovery induced by raised extracellular Ca++ and K+. In addition, Na+/K+ adenosine 5' triphosphatase inhibitors reversed the inhibitory effects of high extracellular Ca++ and K+. Our results suggest that barrier recovery requires both Ca++ and K+ fluxes and are consistent with the hypothesis that both verapamil or dihydropyridine-sensitive Ca++-permeable channels and Ca++-sensitive K+ channels participate in epidermal permeability barrier homeostasis.

Animals↗

PubMed1994

Occlusion lowers cytokine mRNA levels in essential fatty acid-deficient and normal mouse epidermis, but not after acute barrier disruption.

Acute disruption of the permeability barrier by either tape stripping or acetone treatment and chronic disruption by feeding an essential fatty acid-deficient diet increase the mRNA levels of tumor necrosis factor-alpha (TNF alpha), interleukin (IL)-1 alpha, IL-1 beta, IL-1ra, and granulocyte/macrophage-colony-stimulating factor in murine epidermis. Furthermore, epidermal TNF alpha protein levels also are stimulated by barrier disruption. To understand the relation of epidermal cytokine production to barrier function, we studied the effect of the application of a water vapor-impermeable membrane on epidermal cytokine production both in normal epidermis and after barrier disruption. Latex occlusion of essential fatty acid-deficient mice for 24-48 h lowered the mRNA levels of epidermal TNF alpha, IL-1 alpha, and IL-1ra to nearly control values, but not the levels of IL-1 beta mRNA. Occlusion of normal mice for 8, 24, and 48 h did not alter the levels of epidermal mRNAs encoding TNF alpha, IL-1 beta, or IL-1ra. Yet mRNA levels of IL-1 alpha, the major constitutively produced epidermal cytokine, were reduced by 40% after 24 h and by 80% after 48 h of occlusion of normal mouse epidermis. In contrast, latex occlusion of mice immediately after acute barrier disruption by either tape stripping or acetone treatment blocked neither the stimulation of epidermal mRNAs for TNF alpha, IL-1 alpha, IL-1 beta, or IL-1ra, nor the increase in epidermal TNF alpha protein. Taken together, these results suggest that barrier status regulates the production of specific cytokines in essential fatty acid-deficient and normal mouse epidermis. However, the signals that regulate epidermal cytokine production in response to acute barrier disruption do not appear to be influenced by occlusion.

Animals↗

PubMed1994

Integrity of the permeability barrier is crucial for maintenance of the epidermal calcium gradient.

Prior studies have demonstrated a Ca2+ gradient within the epidermis, with the highest concentration in the outer nucleated layers, disappearance of the Ca2+ gradient when the permeability barrier is acutely disrupted, and reappearance of the Ca2+ gradient in parallel with barrier repair, and disruption of the gradient in psoriasis. These observations suggest that integrity of the permeability barrier may maintain the epidermal Ca2+ gradient. To determine further whether a functional barrier is crucial for maintaining the Ca2+ gradient, we examined Ca2+ distribution by ion-capture cytochemistry in essential-fatty-acid-deficient (EFAD) and topical-lovastatin-treated mice, which display a chronic barrier abnormality. In both models, loss of the Ca2+ gradient occurred due to increased cytosolic Ca2+ in the lower epidermis, which normally displays a paucity of Ca2+. Moreover, artificial barrier restoration for 48 h with a water vapour-impermeable wrap normalized the Ca2+ distribution pattern. Acute barrier disruption also leads to the loss of the Ca2+ gradient, but in contrast with the chronic models, loss of the gradient was due to decreased Ca2+ in the upper epidermis. Occlusion with a vapour-impermeable wrap blocked restoration of the Ca2+ gradient after acute barrier disruption. These results demonstrate that chronic barrier disruption increases Ca2+ in the epidermis, and blockade of water flux normalizes Ca2+ distribution, whereas acute barrier disruption leads to loss of Ca2+, and blockade of water flux prevents the return of Ca2+. We conclude: (i) that the epidermal Ca2+ reservoir is derived from the movement of fluids and Ca2+ across the basement membrane, and (ii) that the integrity of the permeability barrier maintains the epidermal Ca2+ gradient.

Acetone↗

PubMed1994

Barrier function coordinately regulates epidermal IL-1 and IL-1 receptor antagonist mRNA levels.

Disruption of the cutaneous permeability barrier increases mRNA levels for TNF, GM-CSF, IL-1 alpha, and IL-1 beta in the epidermis. We have hypothesized that the cytokines mediate the changes in lipid and DNA synthesis which occur following barrier disruption. To further characterize the cytokine response to barrier abrogation, we examined the levels of epidermal IL-1ra mRNA in two acute models and one chronic model in the hairless mouse. IL-1ra mRNA levels increased shortly after acute disruption of the barrier with acetone, reached a peak at 3-4 h after treatment, and returned to control levels by 8h. These changes in mRNA levels parallel those which occur for IL-1 alpha and beta. Furthermore, IL-1ra mRNA levels were elevated 5-fold and 4-fold, at 2.5 h and 4 h, respectively, following tape-stripping, a second acute model of barrier disruption. Finally, IL-1ra mRNA levels were elevated 2.5-fold in the epidermis of EFAD mice, which have a chronic barrier defect. Thus, the cutaneous response to barrier disruption includes mechanisms which increase IL-1 and IL-1ra mRNA levels in a coordinate manner. The net result provides a regulatory mechanism for controlling the biological effects of increased IL-1 production.

Animals↗

PubMed1994

Role of exogenous oxygen in cutaneous barrier repair.

Occlusion of the skin with a water-vapor-impermeable membrane following disruption of the permeability barrier prevents the epidermal changes which lead to the restoration of barrier function, suggesting that water transit could be an important regulatory signal for barrier repair. However, occlusion with a water-vapor-impermeable membrane also prevents the movement of gases, which could also potentially influence permeability barrier homeostasis. Since O2 is known to have an effect on epidermal cell function, we have determined the effect of gases containing different levels of O2 on barrier repair 6 h following topical treatment of hairless mice with acetone. The disrupted barrier of air-exposed animals (O2 approximately 20%) recovered by 50.8 +/- 3.4% (mean +/- SEM) after 6 h. Under flowing air (O2 approximately 20%), O2/CO2 95/5% and argon (O2 = 0%) the barrier recovered by 43.9 +/- 28, 36.2 +/- 8.5 and 39.2 +/- 4.6%, respectively. These values were not statistically different from each other. The slightly lower levels of recovery at 6 h with the flowing gases in comparison to exposure to static air probably can be attributed to a slight cooling of the skin caused by the flowing gases. These results suggest that exogenous O2 is neither required for barrier repair nor a signal for barrier repair.

Animals↗

PubMed1994

Effect of endotoxin and cytokines on lipoprotein lipase activity in mice.

Endotoxin (lipopolysaccharide [LPS]) stimulates the production of cytokines, which mediate many of the metabolic effects associated with infection. In LPS-sensitive C57B1/6 mice, LPS doses as low as 0.01 micrograms per mouse decreased adipose tissue lipoprotein lipase (LPL) activity by greater than 50%. In LPS-resistant C3H/HeJ mice, which do not produce cytokines in response to LPS, doses of LPS as high as 10 micrograms per mouse did not affect LPL activity in adipose tissue. In muscle of C57Bl/6 mice, LPL activity was decreased by 27% after 10 micrograms of LPS, whereas in C3H/HeJ mice there was no effect. These results indicate that the LPS-induced decrease in both adipose and muscle LPL activity is mediated by cytokines. Tumor necrosis factor (TNF), interleukin (IL)-1, leukemia-inhibiting factor (LIF), interferon alfa, and interferon gamma all decreased adipose tissue LPL activity in intact mice. In skeletal and cardiac muscle, only IL-1 and interferon gamma decreased LPL activity, whereas TNF, LIF, and interferon alfa had no effect. Inhibition of TNF activity blocked the increase in serum triglycerides that is characteristically observed after LPS but did not affect the ability of LPS to decrease adipose tissue LPL activity. Inhibition of IL-1 activity with IL-1 receptor antagonist partially inhibited the increase in serum triglycerides; however, the ability of LPS to decrease LPL activity in either adipose or muscle tissue was not affected. These data indicate that although TNF and IL-1 play a role in mediating the increase in serum triglyceride levels, these cytokines do not play a crucial role in the inhibition of either adipose or muscle LPL activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Oxidized lipids in the diet are a source of oxidized lipid in chylomicrons of human serum.

We examined whether oxidized lipids in the diet determine the levels of oxidized lipid in human postprandial serum chylomicrons. After we fed subjects control corn oil containing low quantities of oxidized lipid, the levels of conjugated dienes in the chylomicron fraction were low (9.67 +/- 0.92 nmol/mumol triglyceride), and no thiobarbituric acid-reactive substances (TBARS) could be detected. However, when subjects were fed a highly oxidized oil, the conjugated diene content in chylomicrons was increased 4.7-fold to 46 +/- 5.63 nmol/mumol triglyceride, with 0.140 +/- 0.03 nmol TBARS/mumol triglyceride. When subjects were fed medium-oxidized oil, the degree of oxidation of the chylomicron lipids was moderately increased (21.86 +/- 2.03 nmol conjugated dienes/mumol triglyceride). Additionally, we found that chylomicrons isolated after ingestion of oxidized oil were more susceptible to CuSO4 oxidation than chylomicrons isolated after ingestion of the control oil. The lag time for oxidation decreased from 4.30 +/- 0.40 to 3.24 +/- 0.51 hours (P < .05). These data demonstrate that in humans dietary oxidized lipids are absorbed by the small intestine, incorporated into chylomicrons, and appear in the bloodstream, where they contribute to the total body pool of oxidized lipid.

Adult↗