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Lipid Metabolic Dose Response to Dietary Alpha-Linolenic Acid in Monk Parrot (Myiopsitta monachus)
Lipid Metabolic Dose Response to Dietary Alpha-Linolenic Acid in Monk Parrot (Myiopsitta monachus)
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Lipid Metabolic Dose Response to Dietary Alpha-Linolenic Acid in Monk Parrot (Myiopsitta monachus)
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Lipid Metabolic Dose Response to Dietary Alpha-Linolenic Acid in Monk Parrot (Myiopsitta monachus)
Lipid Metabolic Dose Response to Dietary Alpha-Linolenic Acid in Monk Parrot (Myiopsitta monachus)

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Lipid Metabolic Dose Response to Dietary Alpha-Linolenic Acid in Monk Parrot (Myiopsitta monachus)
Lipid Metabolic Dose Response to Dietary Alpha-Linolenic Acid in Monk Parrot (Myiopsitta monachus)
Journal Article

Lipid Metabolic Dose Response to Dietary Alpha-Linolenic Acid in Monk Parrot (Myiopsitta monachus)

2014
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Overview
Monk parrots ( Myiopsitta monachus ) are susceptible to atherosclerosis, a progressive disease characterized by the formation of plaques in the arteries accompanied by underlying chronic inflammation. The family of n-3 fatty acids, especially eicosapentaenoic acid (20:5n-3, EPA) and docosahexaenoic acid (22:6n-3, DHA), have consistently been shown to reduce atherosclerotic risk factors in humans and other mammals. Some avian species have been observed to convert α-linolenic acid (18:3n-3, ALA) to EPA and DHA (Htin et al. in Arch Geflugelk 71:258–266, 2007 ; Petzinger et al. in J Anim Physiol Anim Nutr, 2013 ). Therefore, the metabolic effects of including flaxseed oil, as a source of ALA, in the diet at three different levels (low, medium, and high) on the lipid metabolism of Monk parrots was evaluated through measuring plasma total cholesterol (TC), free cholesterol (FC), triacylglycerols (TAG), and phospholipid fatty acids. Feed intake, body weight, and body condition score were also assessed. Thus the dose and possible saturation response of increasing dietary ALA at constant linoleic acid (18:2n-6, LNA) concentration on lipid metabolism in Monk parrots ( M. monachus ) was evaluated. Calculated esterified cholesterol in addition to plasma TC, FC, and TAG were unaltered by increasing dietary ALA. The high ALA group had elevated levels of plasma phospholipid ALA, EPA, and docosapentaenoic acid (DPAn-3, 22:5n-3). The medium and high ALA groups had suppressed plasma phospholipid 20:2n-6 and adrenic acid (22:4n-6, ADA) compared to the low ALA group. When the present data were combined with data from a previous study (Petzinger et al. in J Anim Physiol Anim Nutr, 2013 ) a dose response to dietary ALA was observed when LNA was constant. Plasma phospholipid ALA, EPA, DPAn-3, DHA, and total n-3 were positively correlated while 20:2n-6, di-homo-gamma-linoleic acid (20:3n-6Δ7), arachidonic acid (20:4n-6), ADA, and total n-6 were inversely correlated with dietary en% ALA.