The effects of maternal dietary conjugated linoleic acid on embryonic and post-hatch development in an avian model. Vanessa Anne. Leone

ISBN: 9781109476095

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197 pages


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The effects of maternal dietary conjugated linoleic acid on embryonic and post-hatch development in an avian model.  by  Vanessa Anne. Leone

The effects of maternal dietary conjugated linoleic acid on embryonic and post-hatch development in an avian model. by Vanessa Anne. Leone
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A considerable amount of research has been published on the effects of conjugated linoleic acid (CLA, a group of positional and geometric isomers of 18:2(n-6), added as a 50:50 mixture of cis-9, trans-11 and trans-10, cis-12 CLA) on body and fattyMoreA considerable amount of research has been published on the effects of conjugated linoleic acid (CLA, a group of positional and geometric isomers of 18:2(n-6), added as a 50:50 mixture of cis-9, trans-11 and trans-10, cis-12 CLA) on body and fatty acid composition of growing animals, including mice, rats, pigs, and chicks. Maternal feeding of CLA has been shown to also affect the growth, body composition, and fatty acid profile of tissues in the progeny of mothers fed CLA, possibly through inhibition of enzymes involved in lipid metabolism, such as lipoprotein lipase (LPL), stearoyl-CoA desaturase (SCD-1), carnitine 0-palmitoyltransferase (CPT-1), and acyl coenzyme A: cholesterol acyltransferase (ACAT).

We have shown that inclusion of 0.5% CLA into a high fat laying hen diet with two types of additional fat sources, safflower oil and olive oil, modulated growth, body composition, and fatty acid profile of three-week-old chicks in comparison to chicks hatched from mothers fed control diets (no CLA). Previous experiments showed that inclusion of CLA into a low-fat laying hen diet resulted in complete loss of hatchability.

It has been hypothesized that CLA led to an increase in saturated fatty acids (SFA) and a decrease in monounsaturated fatty acids (MUFA) in the egg yolk as well as surrounding vitelline membrane through inhibition of hen SCD-1. When stored at temperatures below 18°C, the membrane became leaky, which allowed minerals to flow across the membrane down their concentration gradients, and resulted in embryonic mortality in fertile eggs.

This phenomenon could be rescued by incorporation of added dietary fat containing high levels of MUFA or polyunsaturated fats. We discovered that in the absence of vitelline membrane disruption (no cooling of eggs prior to incubation) embryos exposed to CLA via maternal diet died. Mortality was not linked to incorporation rate of CLA into the egg yolk fatty acid profile. Mortality in embryos from CLA-fed hens appeared to be linked to the embryos inability to transport lipid from the yolk sac membrane to the developing embryo in the last week of development resulting in less available energy for tissue growth and maintenance.



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