Articles 51-60

Feeding practices in the German BSE epidemy: a preliminary survey of the first 65 Bavarian cases

M. Clauss, E. Kienzle

Institute of Animal Physiology, Physiological Chemistry and Animal Nutrition, Veterinaerstr. 13, 80539 Munich,

It is generally accepted that bovine spongiform encephalopathy (BSE) is transmitted by oral infection via the ingestion of contaminated material. Due to the nature of the potentially infectious agent and the physiological changes of the intestine during the ontogeny of cattle, the reported incubation periods, and the average age at which the disease is clinically observed, it is assumed that infection must take place in young calves, and calf feeding practices therefore have attracted particular attention. We evaluated data from an epidemiological survey initiated by the Bavarian State Ministry of Health, Consumer Protection and Nutrition from the first 65 reported BSE cases in Bavaria. During the survey, the owners of the affected farms were asked a series of questions on the feeding practice, and asked to hand in documentation from which animal feed purchases could be traced back as far as possible, up to 5-6 years previously. In 3 % of the cases it was claimed that the affected animal had not received a milk replacer (MRP). In 58 % of the cases a concentrate had been fed to calves that later became affected. 22 % of the affected animals had received MRP and no concentrates when calves. In one case it was claimed that neither MRP nor concentrates had been used. In more than half of the cases in which MRP only was used, and no additional mineral supplement given. Similarly, in half of the cases in which MRP was used exclusively, no other commercial feed for another animal species (e.g. pigs, poultry) had been purchased. Unless the incubation period of BSE is overestimated at present, these results strongly suggest that milk replacer should be considered as a potential source of BSE infection, and should be further investigated.

Crib-biting in foals is associated with gastric ulceration and mucosal inflammation

A.J. Waters*, C.J. Nicol*, A.D. Wilson*, P.A. Harris** and H.B. Davidson**

*Department of Clinical Veterinary Science, University of Bristol, Langford BS40 5DU, United Kingdom.
**Equine Studies Group, Waltham Centre for Pet Nutrition, LE14 4RT, United Kingdom.

Crib-biting is a stereotypic behaviour performed by approximately 5% of captive domestic horses. Risk factors for crib-biting, identified in recent epidemiological studies, include feeding high concentrate and/or low forage diets (Waters et al., 2002). Experiments have shown that such diets are likely to result in increased gastric acidity (Murray and Eichorn, 1996., Nadeau et al., 2000). We therefore propose that young horses initiate crib-biting in an attempt to produce alkaline saliva to buffer their stomachs when alternative opportunities for mastication are limited. The aim of this study was to determine whether there was an association between crib-biting behaviour and stomach condition in foals. Foals that had recently started to perform crib-biting were recruited into the study and compared with nonstereotypic foals. The stomachs of 15 crib-biting foals and 9 normal foals were examined using a video endoscope. Foals were then randomly allocated to a control or an antacid diet for a 3 month period. Behaviour was monitored by direct observation throughout the 3 month period, and foals re-endoscoped at the end. Videos were scored blind by an independent observer.

Crib-biting foals had significantly more inflamed, dry and ulcerated stomachs than normal foals on first examination (Mann-Whitney: U = 36; N1 = 15; N2 = 9; p < 0.05). Their stomachs also lacked normal folding on first examination, and were significantly smoother when re-examined (Mann-Whitney: U = 11.5; N1 = 12; N2 = 7; p < 0.01). Foals that received the antacid diet had fewer ulcers at the end of the trial (Mann-Whitney: U = 27.5; N1 = 13; N2 = 9). Most foals showed a reduction in crib-biting following treatment but the reduction was more pronounced in foals that received the antacid diet, and reduction in cribbiting correlated with reduction in ulceration (Rank correlation: r = 58; N = 12; p = 0.05). We suggest that the stomachs of crib-biting foals were exposed to more acid conditions or were more sensitive to normal acidity levels than the stomachs of normal foals. The results of this study support the hypothesis that the initiation of oral stereotypy can be a response to a disturbance of the normal digestive process.

Murray, M.J. and Eichorn, E.S. (1996) Effects of intermittent food deprivation, intermittent food deprivation with Ranitidine, and stall confinement with free access to hay on gastric ulceration in horses. Am. J. Vet. Res. 11, 1599 - 1603.
Nadeau, J. A., Andrews, F.M., Mathew, A.G., Argenzio, R.A., Blackford J.T., Sohtell M., Saxton A.M. (2000) Evaluation of diet as a cause of gastric ulcers in horses. Am. J. Vet. Res. 61, 784 - 790.
Waters, A.J., Nicol, C.J. and French, N.P. (2002) Factors influencing the development of stereotypic and redirected behaviour in young horses: the findings of a four year prospective epidemiological study. Eq. Vet. J. (in press).

Deaths in horses caused by ingestion of a hay contaminated by bracken fern (Pteridium aquilinum)

Petra Wolf1, T. Janetzko2, S. Aboling3 and J. Kamphues1

1Institute of Animal Nutrition, School of Veterinary Medicine Hannover, Bischofsholer Damm 15, D-30173 Hannover,
2 Veterinary Practice Varrelbusch,
3 Institute for Botany, University of Hannover

Poisoning due to bracken fern (Pteridium aquilinum) was reported many years ago (1). The intensification of grassland management and optimizing husbandry and feeding conditions means this toxication seems to be mainly in the past. However, ingestion of bracken fern is still possible, when hay is harvested from extensively cultivated areas, fallows near to forests or horses are kept on ‘forest’ pasture.

Case re port
When offered a new batch of hay two of five horses in France showed acute colic symptoms as well as a strong diarrhea. One mare had a miscarriage. Both horses died within a few days after feeding on the hay. Two weeks later, a third horse showed heavy convulsions and colic symptoms and died, too.

Nutritional history:
The ration of the horses was based on hay, supplemented with concentrates and minerals. Because the last feedstuffs were unchanged, the roughage (hay, straw as bedding material) was suspected. These feedstuffs were characterized macroscopically as being of a good quality. The microbiological status of hay and straw was slightly reduced (especially content of moulds):

CFU/g aerobe bacteria moulds Yeasts Hay 4.5 x 105 4.5 x 104 < 103
Straw 4.5 x 104 1.0 x 105 n.d.
The predominant finding was a high contamination with bracken fern (Pteridium aquilinum): > 250 g/kg hay.

Bracken fern contains the enzyme thiaminase, prussic acid containing glycosids and the saponine, pteridin. The highest level of these toxins can be found in fresh leaves, but also in older and dry leaves or in hay containing bracken fern. These toxic ingredients cause ataxia, motor disorders, bloody diarrhea as well as heavy bleeding from nose and mouth or convulsions, although clinical symptoms are different between cattle and horses. Whereas in horses, signs like ataxia or convulsions dominate (due to the vitamin B1 destroying thiaminase), in cattle (which are capable of synthesizing vitamin B1 ) clinical signs are chronical haematuria or ‘bloody sweat’. In the case presented, the reduced microbiological status of hay has to be considered too, and pathogenic symptoms were most prominent as convulsions and colic.

This case report shows that roughage, harvested from extensive areas or fallow, should be proofed critically with regard to both microbiological status and poisonous plants, or plants with toxic constituents (secondary ingredients), before it is provided to horses and cattle.

(1) ROSENBERGER, G. (1978): Diseases in cattle. Parey, Berlin, Hamburg, 2nd edition

The influence of the ratio of structured/unstructured feed on oral disturbances in captive giraffids

J. Hummel1, M. Clauss2, E. Baxter3, E.J. Flach4, K.Johansen5, L. Kolter1

1Zoological Garden of Cologne, Germany
2Institute of Animal Physiology, Physiol. Chemistry and Animal Nutrition, Munich, Germany
3Animal Welfare Research Group, University of Edinburgh
4Institute of Zoology, Whipsnade Wild Animal Park, Dunstable, UK
5Zoo Copenhagen, Denmark

Oral disturbances such as tongue playing, are a common problem in zoo okapis and giraffes. In domestic animals these behaviours often have been associated with feeding practices: diets low in structured feeds (roughage like hay, browse, silage, grass) have been shown to make cattle more prone to behaviours like tongue rolling or licking on substrates. In our studies, the behaviour and food consumption of three individual okapis and six giraffes (of which three were kept as a group) were recorded for 10 days each. The diets consisted mainly of lucerne hay ad libitum, smaller amounts of browse and grain based concentrate. For the three okapis, concentrate/roughage intake ratios of 0.9, 1.1, and 2.3 (on DM-basis) were measured. Only the animal with the highest proportion of concentrate performed oral disturbances. The giraffes showed behaviours like tongue playing or wall licking to varying degrees (5-29% of observation time), but the behaviour was documented for all animals. The concentrate/roughage ratio varied between 2.3 and 3.7. A correlation was found between the proportion of intake of unstructured food and the amount of oral disturbances displayed. After dietary manipulation (addition of tannin-containing pellets), the consumption of more unstructured food led to the occurrence of more oral disturbances in the according animals. The results indicate that the ratio of unstructured/structured food is a very important factor in the development of oral disturbances in giraffids. It has to be stressed that all animals had permanent access to good quality lucerne hay. Our data raise the question of the acceptance of roughage and requirements for structured foods of wild ruminants, especially that of browsers.

Digestive tolerance of sorbitol in cats

Géraldine Blanchard, Marie-Hélène Saniez*, Daniel Wils*,

Bernard-Marie Paragon ENVA - Nutrition - F-94704 Maisons Alfort cedex - *S.A. Roquette Frères - F-62080 Lestrem

Sorbitol is a natural polyol also produced industrially by catalytic hydrogenation of glucose. Although sorbitol is commonly used in semi-humid petfood industry, especially as a humectant, very little information is available concerning its digestive tolerance in cats. This preliminary study was designed to observe the consequences on faeces quality, of different doses of sorbitol (Table 1) in a dry commercial food for cats in order to find a safe dose. Table 1 - Sorbitol dose added to the different diets used in the study

S0 S1 S2 S3 S4
Sorbitol (%) 0 0.25 0.5 1 2 dose (mg/kgBW/d) 0 35 70 140 280

Ten queens, all neutered and receiving the same food (Hill's Feline Maintenance Adult chicken, Hill's Pet Nutrition, Topeka, KS) for several months, were randomly assigned to group A or B, with 5 animals in each group. The experimental design is described in Table 2:

Table 2 - Design of the study (each cell represent a week ; the grey bar between 2 diets, represents a 2 days dietary transition).
Group A S0 S1 S1 S0 S3 S3 S0
Group B S0 S2 S2 S0 S4 S4 S0
Feces Scoring x x x

The queens were housed in individual cages, with paper in the litter box in order to facilitate the collecting of the faeces. The queens had free access to water and received one meal per day at a maintenance amount. The palatability of the food was scored (from 1: very palatable eaten quickly, to 5: very unpalatable). Faeces were collected every morning before the meal, scored for color, texture and odor by the same manipulator, weighed and stored at -20°C until analysis for dry matter, nitrogen content and pH. Statistical analysis consisted of a one way analysis of variance (GLM procedure, SAS system).

Palatability of the food was not modified by sorbitol incorporation. No diarrhea was observed during the entire study. Instead, a slight green coloration of the feces for doses S2, S3 and S4, and a slight softening of faeces in some queens on doses S2 and S4 was noted. However no significant change in the faeces color, odor and texture could be reported, due at least in part to the high individual variation of the results and the small number of animals in each group. No modification of faeces pH, dry matter and nitrogen content and faeces weight could be shown from the doses of sorbitol used in this study. Sorbitol appears to be have tolerated well by the cats at the doses used in this study.

Cats are more sensitive to the toxic effects of oral lipoic acid than humans, dogs, or rats

Ana S. Hill 1, Jonathan A. Werner 2, Quinton R. Rogers 1, Dennis A. Wilson 2, Sharron L. O’Neill 3, and Mary M. Christopher. 3

1 Dept. of Molec. Biosci.,
2 Dept. of Pathology,
3 Dept. of Pathology, Microbiol., and Immunol., University of California, Davis, California, USA

Antioxidant supplementation of pet foods necessitates investigation into safety in target species. Although cats may benefit clinically from antioxidant supplementation to reduce oxidative damage secondary to chronic diseases (e.g. diabetes mellitus or FIV), cats develop clinical toxicity to the antioxidant lipoic acid. This study describes the determination of the maximum tolerated dose (MTD) and toxic effects of a single oral dose of lipoic acid in cats.

Nine healthy adult male cats were housed in metabolism cages in a controlled environment. Three cats received 60 mg/kg lipoic acid (T), three 30 mg/kg (M), and three, no dose (C). Food intake was measured and urine collected. Prior to, 2 hours and 24 hours after dosing, concentrations of serum enzymes, bile acids, ammonia, plasma free amino acids, lipoic (LA) and dihydrolipoic acid (DHLA) were measured and CBCs performed. All cats were euthanized 24 hours after dosing and necropsied. Tissues were assayed for free amino acid, lipoic acid (LA) and dihydrolipoic acid (DHLA) concentrations, and examined histologically using an electron microscope (EM).

By 24 hour after dosing, all T cats showed hypersalivation and ataxia, while T and M cats showed histological and EM hepatocellular changes and significantly increased concentrations of LA and DHLA in plasma, urine, and bile. Gut, liver, pancreas, and kidney LA and DHLA concentrations exceeded those in plasma in T and M cats. Within 2 hours of dosing, serum ALT and ammonia concentrations were significantly elevated while branched chain:aromatic amino acid ratios decreased significantly in the T cats within 2 hours of dosing.

In cats, oral LA produces clinical and hepatocellular toxicity at lower doses than in dogs (126 mg/kg), rats (600 mg/kg), or humans (>2 g/adult). MTD for a single oral dose of LA in cats is < 30 mg/kg. Protein-bound LA and DHLA are primarily excreted in bile, but enterohepatic circulation returns the compounds to the liver. This recirculation could allow accumulation and further metabolism to toxic by-products that interfere with normal cellular metabolism and may trigger apoptosis of hepatocytes.

Effects of dietary clenbuterol and cimaterol on performances, muscle composition and endocrine response in broiler chickens

Schiavone A*., Pagliasso S.**, Tarantola M.*, Perona G.*, Badino P.** and Lussiana C.***

*Department of Animal Production, Epidemiology and Ecology; **Department of Animal Pathology;***Department of Animal Production – University of Turin (Italy).

Dietary administration of beta-adrenergic agonists (e.g. clenbuterol and cimaterol) as energy repartitioning agents in animal nutrition is forbidden in European Countries. In domestic growing animals these molecules bring about an increase in protein deposition and/or a decrease in fat deposition. The effects in birds are less pronounced than in mammals and seem to be more evident in animals either very old or very young and/or to be related to dietary concentration of protein. As illegal administration of beta-adrenergic agonists is assumed to occur in practice, we planned a trial to define the influence of these molecules on male broiler chicken. Fifty-four Ross 508 broiler chicken, 36 days old and of same initial mean live weight, were randomly divided into three experimental groups: control group, clenbuterol group (1 ppm) and cimaterol group (1 ppm). Diets were isonitrogenous and isoenergetic (E.M.: 12.85 MJ/kg; C.P.: 19.20%); animals were fed ad libitum. Body weight and feed consumption were weekly recorded to calculate feed convertio ratio (FCR). At the age of 57 days animals were slaughtered and carcass yields measured. Breast samples were analysed for chemical and fatty acid composition. Testicular androgen receptor (An-R) concentration were measured on cytosol fractions whereas cellular membranes of heart, lung and brain were used to evaluate b-adrenergic receptors (b-AR) levels.

Table 1:
chemical composition of breast muscle
Growth performances (weekly weight gain, feed intake, FCR) and carcass yields were not influenced by dietary treatment even if in clenbuterol group leg weigh was higher (p<0.05). Chemical and fatty acid composition of breast muscle was similar among the groups showing a negligible influence of beta-adrenergic agonists on lipid and protein metabolism in chicken.

Table 2:
b-adrenergic receptors concentration (fmol/mg) (*P<0.05; **P<0.01; ***P<0.001)
Both dietary clenbuterol and cimaterol induced An-R down-regulation in testicular tissue: control 33±2 fmol/mg of protein; clenbuterol 8±0.4 fmol/mg ; cimaterol 8±0.3 fmol/mg.

b-adrenergic receptors concentration in heart, lung and brain are reported in table 2. Data suggest that performances and muscle composition are poorly influenced by dietary administration of beta-adrenergic agonists. It would be useful to analyse the aspects related to endocrine response, as quantification of An-R and b-AR receptors, to identify illegal administration of these molecules.

control clenbuterol cimaterol
Crude protein (%) 22.93±0.659 23.66±0.535 23.60±0.847
Ether extract (%) 1.38±0.274 1.19±0.120 1.39±0.211
Ash (%) 1.18±0.10 1.20±0.05 1.22±0.11
Dry matter (%) 28.29±1.91 26.86±0.87 26.96±0.89
b-AR control b-AR clenbuterol b-AR cimaterol
Heart 244±10 137±11*** 177±18**
Lung 906±16 728±28* 721±75*
Brain 393±28 253±21*** 259±23**

Interaction of dietary unsaturation level with linolenic acid and __tocopherol deposition

Cortinas L.1, Barroeta A.C. 1, Villaverde C. 1, Baucells M.D. 1and Jensen S.K. 2

1Department of Animal and Food Science, Facultat de Veterinària, Universitat Autònoma de Barcelona. E- 08193 Bellaterra, Spain.
2Department of Animal Nutrition and Physiology, Danish Institute of Agricultural Sciences, Research Centre Foulum, DK-8830 Tjele, Denmark.

Over recent years consumers are more aware of the direct repercussion of food on their health. Some works have been studing the meat w3 polyunsaturated fatty acids enrichment, like linolenic acid (C18:3 w3), associated with prevention of cardiovascular diseases. However, the higher unsaturation level in meat leads to an increase in the susceptibility to lipid oxidation. In order to improve oxidative stability of such products, inclusion of tocopherol in animal feeds has been successfully used. Moreover, this supplementation increases the meat vitamin E content. Nevertheless, there are few data regarding the optimum dietary polyunsaturated fatty acids and vitamin E to achieve nutritional benefits in meat. The present study was carried out to evaluate the effect of dietary unsaturation level and supplementation with a-_tocopheryl acetate on linolenic acid and a-tocopherol content in raw poultry breast. One hundred and ninety-six female broiler chickens were randomly distributed into 16 experimental treatments resulting from the combination of 4 levels of dietary polyunsaturated fatty acids (15, 34, 45, 61 g/kg) and 4 levels of supplementation with a-_tocopheryl acetate (0, 100, 200 and 400 mg/kg). The unsaturation degree was achieved by replacing linseed and fish oil to a basal diet enriched with 9% tallow. Linolenic acid content for feed and breast was determined as previously described by Sukhija and Palmquist (1988) and Carrapiso et al. (2000), respectively, using C19:0 as internal standard for the quantification. a-Tocopherol from feed and breast meat was analysed using the method described by Jensen et al. (1999). The dietary polyunsaturated fatty acids clearly affected the linolenic acid content of raw breast meat. Linolenic acid content in breast increased linearly with dietary polyunsaturated fatty acid inclusion of poultry feed (y = 0.1106´ – 0.0021, R2
= 0.73). However, the suplementation with a-tocopheryl acetate did not modify the linolenic acid content in raw breast. a-Tocopherol content of breast meat increased linearly with dietary a-tocopherol supplementation (y = 0.0412´ + 1.1498, R2 = 0.70). Moreover, a-tocopherol content of breast meat was reduced as the inclusion of dietary unsaturation increased. Thus, increasing of 46 g dietary polyunsaturated fatty acid, significantly, decreased 1.86 fold a-tocopherol content in breast of poultry feed with diets supplemented with a-tocopheryl acetate.

Carrapiso A.I. et al., 2000. Meat Sci 56: 159-164.
Jensen S.K. et al., 1999. J Nutrition 129 : 1355-1360.
Sukhija P. and Palmquist D.L., 1988. J Agric Food Chem 36: 1202-1206.

Relationship between dietary PUFA level and apparent absorption of vitamin E in Poultry

C. Villaverde, M.D. Baucells, L. Cortinas, S.M. Martín-Orúe and A.C. Barroeta

Department of Animal and Food Science, Facultat de Veterinària, Universitat Autònoma de Barcelona. E-08193
Bellaterra, Spain

Vitamin E is the major lipid-soluble antioxidant present in nature. Its main function is to protect polyunsaturated fatty acids (PUFA) from peroxidation caused by free radicals. Some old works with rats (Weber et al., 1966, Gallo-Torres et al., 1971) have suggested that dietary PUFA interfere with the intestinal absorption of vitamin E so they increase vitamin E requirements not only because they are easily oxidized and need more protection but also because lower vitamin E intestinal absorption. More recent papers question this fact (Tijburg et al. 1997). The objective of our work was to evaluate to what extent dietary PUFA have an effect in the apparent absorption of a-tocopherol in broiler chickens. One hundred and ninety-six female broiler chickens (8 d) were randomly distributed into 16 experimental groups resulting from the combination of 4 levels of dietary PUFA (15, 34, 45 and 61 g/kg) and 4 levels of supplementation of Vitamin E as a-tocopheryl acetate (0, 100, 200 and 400 mg/kg). The unsaturation gradient was achieved by replacing linseed and fish oil to a basal diet enriched with 9% tallow. A digestibility balance was carried out between days 18 and 22 of age. Feed consumption and total faecal excretion were measured. Faecal samples were collected, lyophilised, milled and stored at -80º C for subsequent analysis. Feed samples were also milled and stored at -80º C. a-tocopherol and a-tocopheryl acetate content in feed and faeces were determined by HPLC using a direct solvent extraction method described by Lee et al. (1999). 1-Phenyldodecane was used as an internal standard for quantification. Total fatty acid content in feed and faeces was determined by GC following transmethylation in methanol-HCl, as described by Sukhija and Palmquist (1988). C19 was used as the internal standard for quantification. The apparent absorption of a-tocopherol was calculated as intake minus excretion of a-tocopherol equivalents (1 mg of all rac a-Tocopheryl acetate = 0.67 mg of d-a-tocopherol) expressed as a percentage of the intake. The apparent absorption of total fatty acids was calculated in the same way. Apparent absorption of a-tocopherol decreased as the level of inclusion of a-tocopheryl acetate in the diet increased (41.7%, 37.4% and 30.8 % for 100, 200 and 400 mg/kg respectively, p£0.05). Dietary PUFA affected apparent absorption of both total fatty acids (47.4% for 15 g/kg vs. 65.9% for 34 g/kg and 74.4% and 78.5% for 45 and 61 g/kg, p£0.001) and a-tocopherol (21.4% for 15 g/kg vs. 40.7%, 42.1% and 42.3% for 34, 45 and 61 g/kg, p£0.001). The low absorption of saturated fat impairs the absorption of other lipidic substances, as it has happened with a-_tocopherol in the tallow-rich diet. Besides this, we couldn’t find any significant difference in a-tocopherol apparent absorption among the rest of unsaturated treatments, suggesting there is no interference of the dietary PUFA level in a- tocopherol uptake in our levels of inclusion. Nevertheless, a possible degradation of a- _tocopherol while protecting PUFA in the gastrointestinal tract should be considered.

Gallo-Torres H.E. et al., 1971. Int J Vitam Nutr Res 41(4): 504-15.
Lee J. et al., 1999. Food Chem Toxicol 64: 968-972.
Sukhija P. and Palmquist D.L. 1988. J Agric Food Chem 36: 1202-1206.
Tijburg L.B.M. et al., 1997. Br J Nutr 77(2): 327-36.
Weber F. et al., 1966. Bibl Nutr Dieta 8:54-63.

Influence of dietary lipid source and genotype on fatty acid composition of Muscovy duck meat

Schiavone A.*, Romboli I.**, Chiarini R.**, Marzoni M.**

*Department of Animal Production, Epidemiology and Ecology – University of Turin;
**Department of Animal Production – University of Pisa - (Italy).

Reported benefits of long-chain polyunsaturated fatty acid (LC-PUFAs), mainly EPA and DHA, on human health have increased the interest in animal products with high level of these molecules. Several studies showed the possibility to modify PUFAs composition of poultry meat by changes in the lipid composition of diet. The aim of this trial was to investigate the possibility to modify meat lipid composition of two different muscovy duck (Cairina moschata domestica L.) strains by dietary strategies. 42 female French broiler strain muscovy ducklings, 35 days old, and 42 female Italian rural strain muscovy ducklings, 42 days old, both of same initial mean live weight were randomly assigned each to two experimental groups (three replications/dietary treatment). The two isoenergetic and isonitrogenous diets (E.M.: 12.5 MJ/kg; C.P.: 16%) differed for lipid source (2% fish oil vs. 2% soybean oil). Breast samples were analysed for fatty acid composition. Multifactorial ANOVA was used to process data; the factors were dietary treatment and strain.

Fatty acid composition of meat was influenced by dietary oil supplementation: fish oil supplementation reduced AA and ALA amount, increased n-3 LC-PUFAs content and n6/n3 ratio was deeply reduced. AA rate was influenced either by dietary treatment or genotype. In conclusion fatty acid composition of duck meat could be easily modified by dietary manipulation. Receptiveness to lipid modification appears very similar between the two examined strains, except for AA which synthesis appeared highest for Italian rural strain.

Fatty acid composition of breast samples (% of methyl esters; mean values ± d.s.) French broiler strain Italian rural strain P level soybean oil fish oil soybean oil fish oil diet strain
C14:0 0.36±0.11 0.42±0.08 0.27±0.01 0.44±0.01 0.05 n.s.
C16:0 23.23±2.16 23.09±0.28 21.92±0.64 22.73±0.52 n.s. n.s.
C16:1n7 1.02±0.35 0.97±0.18 0.68±0.09 0.96±0.18 0.05 n.s.
C18:0 14.76±2.09 15.21±0.78 16.23±0.46 15.94±0.02 n.s. n.s.
C18:1n9 21.63±6.48 18.62±3.10 17.50±1.73 16.95±0.96 n.s. n.s.
C18:1n7 2.40±0.14 2.77±0.15 2.69±0.23 2.81±0.04 n.s. n.s.
C18:2n6 (LA) 17.96±3.12 15.85±2.44 18.29±1.77 15.03±2.22 0.09 n.s.
C18:3n3 (ALA) 0.37±0.07 0.27±0.04 0.35±0.03 0.24±0.09 0.05 n.s.
C20:0 0.12±0.03 0.14±0.02 0.15±0.01 0.14±0.01 n.s. n.s.
C20:1n9 0.15±0.01 0.25±0.04 0.09±0.07 0.29±0.08 0.05 n.s.
C20:2n6 0.33±0.08 0.25±0.08 0.30±0.04 0.25±0.01 n.s. n.s.
C20:3n6 0.75±0.19 0.74±0.15 0.78±0.03 0.71±0.16 n.s. n.s.
C20:4n6 (AA) 9.97±2.40 7.97±0.72 12.88±1.44 9.57±0.71 0.05 0.05
C20:5n3 (EPA) - 1.76±0.20 - 1.67±0.18 - -
C22:5n3 (DPA) 0.57±0.21 1.42±0.24 0.62±0.27 1.46±0.43 0.01 n.s.
C22:6n3 (DHA) 0.70±0.13 6.56±1.39 1.21±0.10 7.36±1.31 0.01 n.s.
SFA 38.76±1.87 39.23±0.90 38.93±0.45 39.72±0.61 n.s. n.s.
MUFA 25.70±6.52 23.27±3.23 21.37±1.91 21.68±1.38 n.s. n.s.
PUFA 34.61±5.38 36.44±2.81 38.98±1.43 37.84±0.81 n.s. n.s.
n6 23.00±3.23 18.46±2.55 23.92±0.63 17.53±1.76 0.05 n.s.
n3 11.61±2.65 17.98±1.86 15.06±1.75 20.31±2.31 0.05 n.s.
n3/n6 0.50±0.09 0.99±0.17 0.63±0.09 1.18±0.26 0.01 n.s.