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Greater Banjul Area, The Gambia.To conduct a pragmatic evaluation of the Xpert(®) MTB/RIF assay in the diagnosis of tuberculosis (TB) among child contacts.In this prospective study, one induced sputum sample was obtained from TB contacts aged15 years and tested using fluorescent microscopy, culture and Xpert. The diagnostic accuracy of the microbiological tests was evaluated against culture and 'all TB diagnosis and treatment' as separate reference standards.Using culture as a reference standard, Xpert was positive for Mycobacterium tuberculosis in 6/14 culture-positive and 6/473 culture-negative children, giving a sensitivity and specificity of respectively 42.9% (95%CI 17.7-71.1) and 98.7% (95%CI 97.2-99.5). With 'all TB diagnosis and treatment' as a composite reference standard, combined Xpert and culture tests were positive for M. tuberculosis in 20/62 children with TB disease (32.3%, 95%CI 20.9-45.3), which was comparable to the yield from microscopy, culture and Xpert combined (33.9%, 95%CI 22.3-47.0), but significantly higher than individual yields from each test.The sensitivity of Xpert is low in actively traced child contacts, but a combination of Xpert and mycobacterial culture has incremental benefits for the bacteriological confirmation of TB disease.

The effects of restricted food intake and acute inflammation on the small bowel were studied, Wistar rats (250 g) were given subcutaneous injections of turpentine (TR) and compared to two control groups, at 18, 42 and 66 h. One was fed ad libitum (C), the other was pair fed (PF) with TR. The TR and PF rats showed hypoplasia of the jejunal mucosa with decreased protein and DNA contents at 42 h and 66 h. The hypoplasia resulted in a reduced villus height that was significantly different from the controls at 66 h (C: 468 +/- 17, TR[66] : 376 +/- 20, PF[66] : 258 +/- 2.9 microm, P0.001). This decrease in villus height was significantly greater in the PF rats than in the TR rats at 66 h. The crypt height/villus height (C/V) ratio in the PF rats was greater than in the TR group at all times. However, the protein and DNA contents in the TR group were significantly higher than in the PF group at 42 h and 66 h (TR/PF[42] : 29.5 +/- 1.9 vs 20.5 +/- 2.0, P0.001, [66]: 25.8 +/- 2.0 vs 16.6 +/- 1.3 mg/10 cm, P,0.001). Disaccharidase activities (sucrase and glucoamylase) per 10 cm jejunum at 66 h were significantly lower in the PF group than in the control and TR groups (sucrase mU/10cm[66] C : 3090 +/- 144, TR 2683 +/- 479, PF 1969 +/- 144, P,0.001; glucoamylase mU/10 cm[66] 237 +/- 25, TR 169 +/- 40, PF 123 +/- 5, P0.01). The N-aminopeptidase patterns in the TR and PF groups were similar. These data suggest that dietary restriction during acute inflammation is the main factor causing hypoplasia of the jejunal mucosa. However, acute inflammation has a trophic effect on the morphological and function of the mucosa. This effect is probably due to inflammatory mediators, whose synthesis is stimulated by turpentine.

Acute inflammation induces changes in liver proteins with an increase in synthesis of positive acute-phase proteins such as alpha1-acid glycoprotein (alpha1-AGP) and a decrease in synthesis of negative acute-phase proteins such as albumin. This is associated with muscle wasting, mediated by increased proteolysis and impaired protein synthesis. As protein metabolism can be altered in other situations (malnutrition, growth) by the form of the dietary nitrogen, we studied the effects of the molecular form of nitrogen on liver and skeletal muscle adaptation, looking at gene expression for two acute-phase proteins (albumin and alpha1-AGP) and a number of muscle proteins (alpha1-actin, ubiquitin and C9 proteasome subunit). Two groups of 24 Wistar rats (250 g) were injected S/C with 0.125 ml turpentine/rat and were fed one of two liquid diets. These diets had caloric, nitrogen, carbohydrate and lipid content but differed in the molecular form of the nitrogen source (whole protein [WP] versus peptide hydrolysate [PH]). Liver and muscle adaptation were studied at 18, 42 or 66 h after turpentine injection. Weight, deoxyribonucleic acid and protein content of the liver were significantly higher with the WP diet than with the PH diet at 42 h and 66 h. There was more alpha1-AGP messenger ribonucleic acid (mRNA) at 18 h and less albumin mRNA at 42 h. Thus, the PH diet causes a more rapid increase in alpha1-AGP mRNA content and a smaller decrease in albumin mRNA content after turpentine injection than the WP diet. However, the changes in plasma acute-phase proteins (albumin and alpha1-AGP) were similar with the two diets. In skeletal muscle, there was no change in mRNA levels for the C9 proteasome subunit at any time point with both diets compared to the controls. However, there were greater ubiquitin mRNA levels at 18|h and less alpha-actin mRNA levels at 18 h, 42 h and 66 h following turpentine injection in the two dietary groups than in the controls. These results suggest that the molecular form of nitrogen ingested regulates hepatic gene transcription or mRNA stability of acute-phase proteins, during the early period of inflammation, but did not affect the expression of muscle proteins, which was altered by turpentine injection. Post-transcriptional control of acute-phase protein genes may contribute to the maintenance of similar plasma levels.

We have investigated the possibility of using 13C-NMR spectroscopy to detect carbon-specific 2H enrichment in dihomo-gamma-linolenic acid and in rat liver lipids. Dihomo-gamma-linolenic acid was chemically synthesized with 98% 2H enrichment specifically at C-18 and C-19 as verified by mass spectrometry and 2H-NMR. Due to a tenfold increase in spin-lattice relaxation time, the C-18 and C-19 peaks normally present at 31.38 and 22.43 ppm, respectively, were not visible in 13C-NMR spectra of [18,18,19,19-2H]-dihomo-gamma-linolenic acid acquired at 1-s pulse repetition rates. However, at 20-s pulse repetition rates, these peaks were both visible as small quintets. This observation was applied to study the effect of deuteration on 13C-NMR peak heights of rat liver fatty acids after consumption of deuterated water. At 1-s pulse repetition rates, 2H enrichment in rat liver total lipids suppressed 13C-NMR signals from acyl carbons except at specific carbons where 2H could not be inserted (mostly in the methyl terminal region and doubly allylic carbons of polyenes). This methodology may therefore have application in the carbon-by-carbon study of fatty acid synthesis and/or degradation.

Objective: To evaluate α-linolenic acid (ALA) (18∶3 n-3) and linolenic acid (LA) (18∶2 n-6) in cholesterol esters (CE) as markers of ALA and LA dietary intakes in preterm infants. Subjects: Forty-five preterm infants: two groups fed different formulas, the third fed human milk. Design: ALA and LA dietary intakes were precisely recorded in each infant to accurately determine the cumulative amount of ingested ALA and LA during two intervals: (i) between the second day after the first significant formula intake (D0) and the fifteenth day (D15); and (ii) between D0 and the first day of the 37th week of post-conception age (W37). The corresponding amounts of ingested ALA and LA were related to ALA and LA levels determined by capillary column gas–liquid chromatography in plasma cholesterol esters at D15 and W37, respectively. Results: ALA in CE was very significantly correlated to D0–D15 and D0–W37 ALA intakes (0.66; P=0.0001 and 0.70; P=0.0001), respectively. LA in CE was weakly correlated to D0–D15 LA intakes (0.03; P=0.01) and whatever the group (human milk or enriched formula) the correlation was lost at W37. Conclusion: In preterm infants, ALA in CE can be considered as representative of ALA dietary intakes, whereas LA in CE appears as a poor marker of LA intakes. European Journal of Clinical Nutrition (2000) 54, 840–843

To investigate the effects of a milk formula supplemented with a alpha-linolenic acid (ALA) (18:2 n-6/18:3 n-3 ratio near 6/1) on plasma and red blood cell (RBC) fatty acids (FAs) in premature infants and compare with a non supplemented formula (18:2 n-6/18:3 n-3 = 22/1).Infants of mothers who elected not to breast-feed were randomly assigned to either a high alpha linolenic formula (HLF: n = 31) group or a low alpha-linolenic formula (LLF: n = 32) control group. Infants fed human milk (HM: n = 25) were enrolled concurrently as a reference group. Anthropometric and biological measurements were made after two days (D2) and 15 d (D15) of enteral feeding and at the 37th week (W37) of postconceptual age. In HLF, the 18:3 n-3 content was 1.95% of total FAs (0.77% of total energy) and the 18:2 n-6/18:3 n-3 ratio was near 6/1. In LLF, the 18:3 n-3 content was 0.55% of total FAs (0.22% of total energy) and the 18:2 n-6/18:3 n-3 ratio was 22/1.ALA supplementation had minimal effect on the n-6 series, did not alter the anthropometric data and confirmed the conversion of ALA into docosahexaenoic acid (DHA). Throughout the study, it maintained, the RBC membrane DHA values within the confidence interval of those obtained in the HM group. Such was not the case with LLF CONCLUSION: alpha-linolenic acid supplementation (from Rapeseed oil and in a 18:2 n-6/18:3 n-3 ratio = 6) in premature infant formula can contribute efficiently to the maintenance of the n-3 status in the premature newborns.

Summary - Bovine whey proteins such as œ-lactalbumin and ~-Iactoglobulin are with bovine caseins the most commonly used proteins in infant formulas owing to their high nutritional value. However, these cow milk components are not always weil tolerated and can induce allergies in infants. The purpose of this study was therefore to investigate the gastric (pepsin) and pancreatic (trypsin, chymotrypsin and elastases 1 and II) enzymatic hydrolysis of ~-Iactoglobulin with the aim of finding a means to reduce its antigenicity. Elastases 1and II were first purified from porcine pancreatic acetone powder. After differential precipitation steps, elastases 1and II were separated by cation-exchange chromatography. The conditions regarding ~-Iactoglobulin hydrolysis by gastric and/or pancreatic enzymes were similar to those used for hypoallergenic milk preparations. Elastase II and to a lesser extent elastase I, were effective in enhancing ~-Iactoglobulin hydrolysis via a mix of pepsin, trypsin and chymotrypsin and in reducing the residual antigenicity ofhydrolytic products. The sarne hydrolytic percentage was observed when elastase 1or II were added, while the residual antigenicity was lower in the presence of elastase II than in the presence of elastase 1.The introduction of elastases in the pancreatic IIUX can therefore be proposed to enhance the hydrolysis of cow milk components in hypoallergenic milk preparations. * Correspondence and reprints ~-Iactoglobulin hydrolysis / pancreatic elastases 1 and II / residual antigenicity / hypoallergenie milk

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Nervous tissues and the retina are rich in docosahexaenoic acid [DHA, C22: 6(n-3)], an essential fatty acid which is the product of the elongation and desaturation of alpha-linolenic acid [alpha-LnA, C18:3(n-3)]. Lower plasma and membrane DHA levels as well as impaired nervous function (psychomotor development, visual disturbances) have been observed in premature babies receiving standard milk products compared to breast-fed babies and have been related to the lack of long-chain (C20) fatty acids in these products. In the present study, we have investigated whether it is possible to increase the plasma and erythrocyte DHA level in premature infants by giving them a milk formula enriched in alpha-LnA (1.95% vs 0.55%). Results showed that, after 15 days of feeding, alpha-LnA supplementation significantly increased plasma DHA availability [2.20 vs 1.54% (p0.0001) in the plasma phospholipids] and increased DHA level in erythrocyte membranes [3.02 vs 2.54% (n.s.) in the red blood cell phosphatidylethanolamines]. At the LA/alpha-LnA ratio used (6/1), there was only a limited impact on the n-6 pathway which was reflected in a slight decrease in the arachidonic acid (AA) of the plasma phospholipids [6.88 vs 7.53% (p0.05) after 15 days]. Furthermore, the AA content of the red blood cell phosphatidylethanolamines was perfectly preserved even after a mean period of 4-5 weeks of feeding [(15.70 vs 14.86% (n.s)]. The observed enhancement in fatty acids of the n-3 series calls for a prospective study investigating whether these improvements are associated with changes in the kinetics of psychomotor development and in the visual function of enriched-formula-fed versus breast-fed babies.

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Seven non-anaesthetized pigs (mean body-weight 64.6 kg) were used to study the intestinal absorption and hepatic metabolism of glucose and amino acids (AA) using carbohydrate solutions (maltose dextrin; 440 g/2 l), containing 110 g of either an enzymic milk-protein hydrolysate (PEP) with a large percentage of small peptides (about 50% with less than five AA residues) and very few free AA (8%) or a mixture of free AA (AAL) with an identical pattern, infused intraduodenally. Each pig was previously fitted under anaesthesia with electromagnetic flow probes around the portal vein and the hepatic artery, and with permanent catheters in the portal vein, carotid artery, one hepatic vein and the duodenum. Each solution was infused for 1 h after a fasting period (18 h) and each pig received both solutions at 8 d intervals. The observation period lasted 8 h. For most AA (his, lys, phe, thr, arg, tyr, pro) the absorption rate after infusion of PEP was significantly higher than after that of AAL during the 1st hour, but the differences quickly disappeared. After 8 h, the only differences concerned his and tyr (PEP > AAL) and met, glu and asp (AAL > PEP). There was a large uptake of blood AA by gut-wall cells, higher after AAL infusion than after PEP infusion, particularly for branched-chain AA (BCAA). The absorption of ammonia-nitrogen after both infusions was equivalent to two-thirds of urea-N passing from blood to intestinal tissues and lumen. Glucose absorbed within 8 h represented only 76% (PEP) or 69% (AAL) of the infused amounts. The cumulative hepatic total AA (TAA) uptake increased from 13 to 27% of the infused amounts between the 1st and the 8th hour after PEP infusion, and from 8 to 31% after AAL infusion. Most essential AA were largely taken up by the liver, with the exception of met (PEP) and thr and of BCAA, which were poorly retained for both solutions; there was a high uptake of ala and gly, and a release of asp, glu, and gln. Urea-N released by the liver within 8 h was equivalent to 23–25% absorbed amino-N and to around 1.5 times ammonia-N taken up by the liver within 8 h. Glucose was highly taken up by the liver during the first hours then released, the total uptake within 8 h representing about half the absorbed amount. There was a lactate release tending to be higher after PEP than after AAL infusion and a liver pyruvate release identical for both solutions. From calculations of net non-catabolic metabolism in the liver the possible synthesis of liver proteins within 8 h may be estimated at 35 g for both solutions. The cumulative peripheral TAA uptake increased from 12 to 27% of the infused amounts between the 1st and 8th hour after PEP and from 9 to 11% after AAL infusion. At 8 h after the infusion the larger uptake concerned BCAA, arg, glu and asp and there was a marked release of gln, gly and ala for both solutions; the peripheral balance was zero for met (PEP) or characterized by a release of phe and thr (AAL). Thus, protein synthesis seemed only to be possible with the aid of plasma proteins synthesized in the liver. The 8 h peripheral balance of glucose, lactate and pyruvate was characterized by the same level of uptake for both solutions. The time-course of AA absorption, depending on the physicochemical structure of nitrogenous mixtures present in the digestive tract, had an influence on the pattern of liver and peripheral AA uptake.

Elastin—triglyceride complexes were prepared in vitro using a swelling solvent, such as dimethylformamide or tertiary butanol, and mixing fibrous elastin with vegetable oils (palm, corn, primrose, olive, sunflower and soya). These elastin-lipid complexes contain from 2.2 × 10 −3 to 6.4 × 10 −2 mmoles of triglycerides per g of elastin. The fatty acid composition of these elastin—lipid complexes depends to some extent on the temperature and on the swelling solvent used in their preparation. With some oils the fatty acid composition of the elastin-lipid complexes differs significantly from that found inn the original oil. Some elastin—lipid complexes such as those prepared with soya oil and primrose oil have an increased resistance to the action of pancreatic elastases compared with the control elastin sample. Although the dried elastin—lipid preparations are quite similar to those of untreated elastin, the elastolysates of such elastin—lipid complexes are turbid and have a similar appearance to lipemic sera, in sharp contrast to the control elastolysates which are perfectly transparent. These results agree with previous claims that elastin—lipid complexes are formed in vivo mainly by hydrophobic interactions between the elastin peptides, rich in aliphatic amino acids, and the lipids. They also enable some of the factors influencing the formation of elastin—lipid complexes to be studied in vitro using nutritionally important vegetable oils and highly purified elastin.

Sixteen old subjects were given daily dietary supplement of lg of linoleic acid and lg of gamma-linolenic acid (primerose oil) or 2g of linoleic acid (sunflower oil) for periods of two months. Haemostatic parameters, platelet aggregation, exogenous and endogenous arachidonic acid metabolism were investigated before and after the intake. Diets did not induce any significant change in haemostatic parameters (bleeding time, levels of anti-thrombin III, plasminogen and plasma B-TG and PF4). Platelet rich plasma aggregation induced by collagen and arachidonic acid were significantly reduced after linoleic acid(18:2n-6)intake. In contrast, gamma-linolenic acid(18:2n-6)supplement did not after aggregation. However, thromboxane B2 formation (under stimulation) and vitamin E level in platelets (but not in plasma) were decreased after 18:3n-6 as compared to 18:2n-6 intake. The mechanism of thromboxane B2 decrease is unclear. Nevertheless, we may speculate that beneficial effect of this decrease could be counterbalanced by the decreased platelet vitamin E. We conclude that intake of 18:2n-6 or 18:3n-6 does not affect much platelet functions in elderly people.

Male rabbits (10 weeks old) were fed, for 20 weeks, purified diets rich in fat (45% of calories) containing saturated fats (butter), polyunsaturated fats (evening primrose oil + butter or sunflower oil + butter) for 20 weeks. Linoleic acid represented respectively 3.6, 33 and 34% of the dietary fatty acids, while gamma-linolenic acid was present (4.4%) solely in the second group. A significant increase in di-homo-gamma-linolenic acid in plasma, platelets and aorta was noted only in the animals fed evening primrose oil. Despite this, the results of the platelet aggregation to thrombin and ADP, the recalcification plasma-clotting time (platelet-rich plasma) and the severity of atherosclerosis were not significantly different from those observed in the group fed sunflower oil. In contrast, in comparison to the butter-fed animals, the two groups fed the polyunsaturated fats showed remarkable improvements in the clotting time (P less than 0.01) and in the severity of atherosclerotic lesions (evening primrose oil P less than 0.001; sunflower oil P less than 0.05). However, the response to thrombin-induced aggregation was significantly decreased (P less than 0.05) only in the evening primrose oil-fed animals. In these long-term studies in young rabbits, dietary gamma-linolenic acid did not seem to have marked beneficial effects, additional to those induced by linoleic acid, on platelet functions or on atherosclerosis.

Male Sprague-Dawley rats were fed during one year with diets containing 12% of one of the following fats: butter, sunflower oil, rapeseed oil, soybean oil, hydrogenated soybean oil, palm oil, canbra oil and arachid oil. Total serum cholesterol was lower in the arachid, suflower and butter groups and higher in the palm and hydrogenated soybean groups (p less than 0.01); serum cholesterol esters were lower in the arachid, sunflower and soybean groups, but higher in the palm and hydrogenated soybean groups ( p less than 0.01). Serum triglycerides were lower in the sunflower and arachid groups and higher in the butter and palm groups (p less than 0.01). There was a positive, significant correlation between serum cholesterol and phospholipids in the various groups. In aortas, free cholesterol levels were the same in different groups, but cholesterol ester levels increased in the following order: canbra, butter, arachid, palm, sunflower, rapeseed, hydrogenated soybean and soybean red groups (p less than 0.01). There was a significant correlation between aorta cholesterol esters and the ratio 18:0 + 18:1 of the dietary fat (r = 0.69; p less than 0.001).

In 260 male farmers (40-45 years) divided into 9 groups from different areas in France and Britain, coagulation, platelet aggregation, lipemia, fatty acids from plasma lipids and platelet phospholipids were determined in relation to the food intake evaluated by recall, weighing and chemical analysis of the diet. The clotting activity of platelets and their response to thrombin aggregation was significantly correlated on an individual basis with the intake of saturated fatty acids both in subsamples as well as in the whole study. Serum cholesterol was also significantly correlated with saturated fats but only on a group basis or on the totality of the study. Calcium, linolenic acid and alcohol in the diet were inversely related to certain platelet functions. Linoleic acid was inversely related to serum cholesterol and triglycerides. Dietary saturated fats were associated, with an increase in the platelet phospholipids not in saturated fatty acids but in 20:3 (n-9), known to promote platelet aggregation to thrombin, with a decrease in platelet cholesterol, also apparently regulating platelet functions. The present studies indicate that dietary saturated fats, calcium (hard water) and alcohol, influence platelet behaviour in a way strictly parallel to their known effect on coronary heart disease.

1. Six non-anaesthetized pigs (mean body-weight 57.0 kg) were used to study the intestinal absorption of amino acids (AA) from either an enzymic hydrolysate of milk (PEP) containing a large percentage of small peptides (about 50% with less than five AA residues) and very few free AA (8%), or from a mixture of free AA with an identical pattern (AAL) infused intraduodenally in one of two amounts (55 or 110 g). Concomitant insulin and glucagon production rates were estimated.2. Each pig was previously fitted, under anaesthesia, with an electromagnetic flow probe. around the portal vein, with permanent catheters in the portal vein, the carotid artery and the duodenum. Each infusion was performed after an 18 h fasting period and each pig received each infusion. The observation period lasted for 5 h.3. The absorption of AA was greater, more rapid and more homogeneous after PEP infusion than after AAL infusion, independent of the amount infused.4. For the majority of AA considered individually, the absorption coefficient was higher after infusion of PEP than after that of AAL. The exceptions were methionine with a higher absorption coefficient after AAL infusion, and isoleucine, aspartic acid + asparagine and glutamic acid + glutamine with identical coefficients for both infusions.5. Some AA, such as asparagine, ornithine, citrulline and taurine, while absent in the infusates, appeared in the portal vein in appreciable amounts after the infusion of both solutions. While a small proportion of taurine may arise from recycling of taurine-containing bile salts, it seems that the gut wall is able to synthesize all four AA.6. Insulin production did not differ according to the nature or amount of solutions infused. Glucagon production was greater after PEP infusion.

In order to gain insight into the mechanism of platelet dysfunction in insulin-dependent diabetics we studied in 17 patients the influence of a 6-week period with a dietary supplement of gamma-linolenate: 2 g/d (group I, n = 8) or 500 mg/d (group II, n = 9). Serum lipids, plasma beta-thromboglobulin (beta TG), platelet aggregation in vitro, and TxB2 and PGE1 released from platelets during the aggregation process were measured. In group I, serum triglycerides fell from 1.57 +/- 0.28 mmol/l to 0.99 +/- 0.17 mmol/l (P less than 0.01) and cholesterol fell from 5.85 +/- 0.55 mmol/l to 5.08 +/- 0.52 mmol/l (P less than 0.01). In group I plasma beta TG fell from 100.0 +/- 15.7 ng/ml to 73.7 +/- 12.1 ng/ml (P less than 0.025), while the sum of the percentages of the C18:3 omega 6 and its chain elongated (C20:3 omega 6) and desaturated (C20:4 omega 6) metabolites increased in serum triglycerides (P less than 0.05), cholesterol esters (P less than 0.02) and phospholipids (P less than 0.02). No changes were observed on the other parameters in either group. The results show that the lowering effects of gamma-linolenate on serum triglycerides, cholesterol and plasma beta TG occur only with daily intakes of 2 g. The changes in fatty acid composition of serum lipids suggest that the gamma-linolenate intake of 2 g may exert its beneficial effect through an increased incorporation of long-chain polyunsaturated fatty acids, but no firm conclusion can be drawn as membrane platelet fatty acid composition was not evaluated.

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33 healthy men, 72 years old on average, ingested during five week: 2,4 g of Oenothera Biennis oil rich in PUFA. Before and after ingestion, platelet aggregation was measured according to the Born's photometric method, which divided the original group into two classes: "15" normal subjects (NAG) and "18" hyperagregated (HAG). The fatty acids contained in the serum were analysed by GLC. NAG liquid pattern did not show any difference after oil ingestion, as in HAG group, significant modifications were observed in palmitoleic, linoleic and linolenic fatty acid series. These observations probably correspond to a fundamental behavior difference, which might be related to desaturase activity reduction. Such a phenomenon would appear with ageing in some subjects. If this hypothesis is confirmed, the inclusion of the two methods of investigation described above would constitute a good approach for studying the enzymatic system activity in ageing.

In a five-day clinical test, the dietary effects of canbra oil and butter on normal human subjects were studied with special reference to lipid metabolism, clotting times and platelet functions. There was no difference between the canbra oil and butter diets as regard triglyceridemia or clotting times, but cholesterolemia and in vitro platelet aggregation by ADP dropped significantly in subjects fed the canbra oil diet. The platelet count did not change significantly. A possible explanation of these results might to be the difference in the fatty acid composition of canbra oil and butter.

Four diets which differed in fatty acid composition were provided for five months each to a group of 24 healthy nun volunteers. The diets contained 54% carbohydrates, 16% proteins and 30% lipids. One-third of the lipid part remained unchanged during the whole study, and two-thirds were modified during each period. For this latter portion, one of the following dietary fats was used: sunflower oil, peanut oil, low erucic acid rapeseed (LEAR) oil or milk fats. This procedure allowed an evaluation of the effects of various amounts of dietary linoleic acid (C18:2 omega 6) and alpha-linolenic acid (C18:3 omega 3) on the serum level of their metabolites. A diet providing a large amount of linoleic acid (14% of the total caloric intake) resulted in low levels of dihomo-gamma-linolenic acid (C20:3 omega 6) and arachidonic acid (C20:4 omega 6) in serum phospholipids and cholesteryl esters. A diet providing a small amount of linoleic acid (0.6% to 1.3% of the total caloric intake) induced high levels of omega 6 fatty acid derivatives. Intermediate serum levels of C20:3 omega 6 and C20:4 omega 6 were found with a linoleic acid supply of about 6.5% of the total caloric intake. Serum levels of omega 6 metabolites were not different after two diets providing a similar supply of C18:2 omega 6 (4.5% to 6.5% of the total caloric intake), although in one of them the supply of C18:3 omega 3 was higher (1.5% for LEAR oil versus 0.13% for peanut oil).(ABSTRACT TRUNCATED AT 250 WORDS)

Four different oils : onager oil, mixture of onager oil (20 p. cent) and middle class triglyceride, sunflower oil and soybean oil were given to the rat during three different periods of time : 1) during 3 months after weaning ; 2) during 6 months after weaning ; 3) from the 9th to 15th months. Three types of myocardial lesions were found : interstitial inflammatory reaction, foci of cellular necrosis and fibrosis. The semi-quantitative study of these lesions did not find important differences from one oil to the other, as well as with the controls. However, subgroups onager are among the least altered, particularly as far as necrotic lesions are concerned. Morphometry of mitochondria, despite evident alterations under electron microscope, gave similar results in every groups.