The Occurrence and Effects of Human Vitamin E Deficiency

Farrell, Philip M.; Bieri, John G.; Fratantoni, Joseph F.; Wood, Robert E.; Sant'Agnese, Paul A. di

doi:10.1172/jci108760

Cited by 237 publications

(72 citation statements)

References 25 publications

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“…Furthermore, there was no difference between the globular resistance of the CF patients and the healthy controls. Therefore, it is not obvious that the changes in FA turnover observed for the CF patients are caused by vitamin E deficiency as described by some investigators (6,10,12). The FA compositions of the RBC , platelet, and plasma lipids for healthy subjects and for CF patient 6 are shown in Table 5.…”

Section: Additional Determinations the Results For Serum Vitamin Ementioning

confidence: 95%

Abnormal Fatty Acid Turnover in the Phospholipids of the Red Blood Cell Membranes of Cystic Fibrosis Patients (in Vitro Study)

Rogiers¹,

Dab²,

Michotte³

et al. 1984

Pediatr Res

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ROGIERS ET AL.young DI rats than in young SO rats and adult DI and SO rats. We also found that this hypotension could be prevented by the continuous infusion of AVP (2000 pg·lOO g-I min-I). The adult 01 rats were more resistant to hemorrhagic hypotension than the infant 01 rats. The reason for this is not known. In addition to AVP, angiotensin has also been thought to prevent hemorrhagic hypotension. The angiotensin levels were the same in the adult DI and SO rats both during control conditions and following bleeding. It is therefore likely that the relative resistance to hemorrhagic hypotension, observed in adult DI rats, is independent of angiotensin.The serum AVP levels were measured in the SO rats. The capacity to release AVP was at least as good in young as in adult rats. Previous studies on fetal lambs have shown that the capacity to release AVP in response to blood volume contraction is well developed even in fetal life (12). The AVP levels recorded under basal conditions were high in both the adult and the infant 01 rats; they were 21 and 45 pg-ml", respectively. In adult rats that have been dehydrated for 48 h, the AVP concentration has been reported to be around 30 pg.ml-I (5). The SO rats in this study had been dehydrated for 10 h and subjected to anesthesia and blood vessel cannulation which might have caused the blood volume contraction. Great care had, however, been taken not to use animals that had been bled prior to carrying out the procedure. Following bleeding, the AVP levels increased in both groups, but the increase was significant only in the adult rats. It is possible, however, that the AVP levels in the infant rats were already so high during basal conditions that they represented maximal levels. SummaryA study was carried out in order to investigate whether the abnormal in vitro turnover of fatty acids in the phospholipids of the red blood cell membranes of cystic fibrosis patients is intrinsic to the membrane, or whether it is induced by extrinsic serum factors. Red blood cells of cystic fibrosis patients and healthy subjects were labeled in vitro with 1 14 q linoleic acid, bound to albumin. The labeled cells were reincubated in autologous and homologous serum. The radioactivity present in the serum lipids and in the major phospholipid fractions of the red cell membranes was measured.Conclusions of this study are: 1) not all of the cystic fibrosis patients examined individually show an abnormal in vitro turnover of the red cell fatty acids, although they all presented abnormal fatty acid patterns for the red blood cell phospholipids,

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Section: Additional Determinations the Results For Serum Vitamin Ementioning

confidence: 95%

Abnormal Fatty Acid Turnover in the Phospholipids of the Red Blood Cell Membranes of Cystic Fibrosis Patients (in Vitro Study)

Rogiers¹,

Dab²,

Michotte³

et al. 1984

Pediatr Res

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“…Analysis of tocopherol (vitamin E) in plasma was carried out by colorimetric methods applied to plasma lipid extracts, as described previously (14); this technique permits simultaneous determination of carotene.…”

Section: Methodsmentioning

confidence: 99%

Correction of Linoleic Acid Deficiency in Cystic Fibrosis

et al. 1986

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ABSTRACT. To identify evidence of essential fatty acid deficiency, we screened 64 patients with cystic fibrosis by analyzing total lipid extracts from plasma. Forty-three had an abnormal linoleate (18:2) level (less than 26%). Thirteen deficient patients (aged 10-24 yr) ingested for 1 yr 7% of their total calories as linoleate derived from a daily supplement of Microlipid. Five deficient patients (aged 10-37 yr) served as controls. Plasma and erythrocyte fatty acid composition were monitored by gas chromatography of total lipid extracts seven times during the twelve month period. Prostaglandins E2 and FZa and their 15 keto 13, 14 dihydrometabolite, 6-keto F,,, and thromboxane B2 were measured by radioimmunoassay. Sweat tests, oxygen saturation, growth indices, clinical severity scores, compliance, and possible side effects from taking Microlipid were followed. Results showed that oral supplementation with Microlipid can significantly increase plasma and erythrocytes %18:2. One compliant patient died during the study and had normal tissue 18:2 levels. Nine of 13 patients gained more weight while taking Microlipid than in the previous year. No significant changes in sweat electrolytes, clinical scores, or oxygen saturation were found during the study year. Prostaglandin metabolites prostaglandin E2 showed an upward trend in supplemented patients, compared to controls. Prostaglandin FZa remained unchanged over 1 yr but showed a trend significantly downward over the final 6 months in supplemented patients. We conclude that linoleate deficiency can be corrected with daily Microlipid supplements and that correction may alter prostaglandin metabolism (Pediatr Res 20: 36-41, 1986) Abbreviations CF, cystic fibrosis 18:2, linoleate PGM, 13,14-dihydro-15-PGFza PG, prostaglandin EFA, essential fatty acid RBC, red blood cells Several workers (1 -3) have demonstrated markedly decreased concentration of essential fatty acid (EFA) in plasma from CF patients. The major changes include a decreased level of the predominant EFA, linoleate (1 8:2), and increased palmitoleate

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“…supplements (i.e. presence of hypocarotenemia, gross steator-(Pediatr Res 19: 104-109, 1985) rhea, and an abnormal fat balance evaluation whenever studied); 11-patients with malabsorption who were supplemented with Abbreviations 100-200 IU of a-tocopheryl acetate in a water miscible form (9); and 111-patients with no evidence of steatorrhea, a normal EFA, essential fatty acid vitamin E status without tocopherol supplements, and normal CF, cystic fibrosis fecal fat excretion (26) and/or plasma carotene level. The age PUFA, polyunsaturated fatty acid ranges of the three groups of patients and a normal group of TLC, thin layer chromatography healthy volunteers were similar; most patients were adolescents or young adults.…”

mentioning

confidence: 99%

Fatty Acid Abnormalities in Cystic Fibrosis

et al. 1985

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hepatic 25-hydroxylation of vitamin D and that alcohol, while having no effect on 25 OH D production in adult livers, inhibits synthesis in pup livers. Alcohol-mediated decreases in pup hepatic 25 OH D production as well as decreases in 25 OH D transport from mother to fetus (13) Printed in U. S. A. Fatty Acid Abnormalities in Cystic Fibrosis PHILIP M. FARRELL, ELAINE H. MISCHLER, MICHAEL J. ENGLE, D. JEANNETTE BROWN, AND SZE-ME1 LAU Departments of Pediatrics and Nutritional Sciences, University of Wisconsin-Madison, Madison, Wisconsin 53792ABSTRACT. Fatty acids were measured by gas chromatography in lipid extracts of plasma and tissues obtained from three categories of 46 patients with cystic fibrosis. Low levels of the major essential fatty acid linoleate were found in plasma total lipids of patients who had malabsorption but not in those without evidence of steatorrhea. Circulating arachidonic acid was only slightly decreased, and the unusual triene reflecting pathologically altered fatty acid metabolism (20:3w9) was generally not detected, nor was the trieneltetraene ratio abnormal except for in Received February 1, 1984; accepted August 24, 1984 of malabsorption, namely plasma carotene (r = 0.64) and fecal fat excretion (r = 0.76). Our data therefore indicate that the abnormality in linoleate is associated with (secondary to) malabsorption of dietary fat despite pancreatic enzyme replacement therapy and consumption of a regular diet. The frequency of this alteration was determined to be quite high in 40 patients with steatorrhea, 85% of whom showed values below the lower limit of normal for plasma linoleate. It was of interest to find markedly decreased levels of linoleate in adipose tissue, cardiac muscle, and lung and lesser reductions in liver and psoas muscle taken at autopsies. Tissue arachidonic acid percentage was normal, however, and 20:3w9 was rarely present. Thus, the physiological significance of this common abnormality in

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The Occurrence and Effects of Human Vitamin E Deficiency

Cited by 237 publications

References 25 publications

Abnormal Fatty Acid Turnover in the Phospholipids of the Red Blood Cell Membranes of Cystic Fibrosis Patients (in Vitro Study)

Abnormal Fatty Acid Turnover in the Phospholipids of the Red Blood Cell Membranes of Cystic Fibrosis Patients (in Vitro Study)

Correction of Linoleic Acid Deficiency in Cystic Fibrosis

Fatty Acid Abnormalities in Cystic Fibrosis

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