Danny A. Flores*

Skye Blue Publications, Port Coquitlam, BC Canada V3B 1G3

*Correspondence address: 1440 Barberry Drive, Port Coquitlam BC Canada

 

 

 

Introduction.

 

As far as has been gleaned from available literature these models are schema with their own mechanisms physiologicaly and genetically to reduce cholesterol deposition in the ova or shell egg of poultry and turkeys as a result.  We will now introduce these in the ff.:  

The Naked Neck and Frizzle Model

There is a model for chickens that indicates for the Naked neck (Na) and Frizzle (F) genes in layers showing that crosses with Nana or Ff and Nana x Ff regulate good versus bad serum cholesterol, viz., high-density lipoprotein cholesterol (HDL-C) versus low-density lipoprotein cholesterol (LDL-C), associated with lowering egg cholesterol concentration (Mahrous and El-Dlebshany, 2011).

It has been demonstrated that addition of 3% fishmeal (FM) improves egg production traits but was not able to reduce cholesterol concentration in the yolk significantly (Rowghani, Boostani, Mahmoodian Fard and Frouzani, 2007).

Restricted Ovulator (R/O) Model

The transgenic manipulation to reverse a gene's point mutation coding for the very low density lipoprotein (VLDL) receptor, a 95-kDa membrane protein which mediates the massive uptake of the main circulating synthesized yolk precursor, VLDL and vitellogenin (VTG), could confirm the effect on the heritable hyperlipidemia and aortic atherosclerosis in the R/O model in chickens (Elkin, Bauer and Schneider, 2012).

Blocking Pancreatic Cholesterol Esterase in a Model of Cholesterol Metabolism

As with chicken meat, turkey has a lower cholesterol content than most other meats, especially red meat. Turkey and chicken should be made an even better choice than these other meats using the poultry model involving pancreatic cholesterol esterase in digestive cholesterol absorption and uptake into tissues, as has been demonstrated with the hamster. Turkey should demonstrate that their inhibition of pancreatic cholesterol esterase reduces cholesterol absorption. These would be accomplished with cholesterol drug analogue inhibitors to block cholesterol esterase function (Heindrich, Canlos, Hunsaker, Deck and Jagt, 2004).

Reducing Shell Egg Cholesterol Using Genetic Approaches

Cholesterol metabolism comprises: 1) cholesterol synthesis, 2) cholesterol elimination, 3) cholesterol transport and 4) cholesterol storage (S. Meany, 2014).  In the Naked neck (Na) and Frizzle (F) phenotypes, cholesterol in high-density lipoprotein (HDL-C) increased and cholesterol in low-density lipoprotein (LDL-C) decreased (Mahrous and El-Dlebshany, 2011). Together with the fact that the very low density lipoprotein (VLDL) receptor, a 95-kDa membrane protein that normally mediates massive uptake of main circulating cholesterol and triglyceride concentrations with normal layers, is point mutated as in the R/O model results in 5-fold elevation in circulating cholesterol and triglycerides concentrations (Elkin, Bauer and Schneider, 2012).

Two technologies are emerging: 1) delivery of transgenes using lentiviral vectors, or 2) "knockdown" (silencing) of gene expression via small interferent RNAs (Elkin, 2007).  One approach with the former is tissue-specific expression of extra copies of the VTG gene or possibly lipvitellin (LV-I) mediating VTG binding to receptors LR8 and LRP380 to increase oocyte uptake of VTG at the expense of "yolk targeted VLDL" or VLDLy, which components of cholesterol and lipid, bind those receptors; also, LR8 specificity might be altered towards binding VTG over VLDLy (Elkin, 2007).  The latter approach would also partially knockdown cholesterol biosynthetic genes (e. g. squalene synthase) or VLDLy assembly or oocyte lipoprotein receptor binding (e. g. MTP, apoVLDL-II or apoB) and could result in a similar reduction in yolk cholesterol content (Elkin, 2007). Lastly, "knockdown" of avian homologue ABCG5 and ABCG8 transporters once identified together with a phytosterol-rich diet which would replace cholesterol in the yolk, unable to oppose absorption of phytosterols from the intestine, and promote their secretion from the liver (Elkin, 2007).

Poultry transgenesis does not address manipulating egg number (i. e. multiparous ovulation), for e. g., via hormonal regulation and reproductive biology at this time.  There is an inverse relationship between egg yolk cholesterol content and rate of egg production (Elkin, 2006)

Reducing Shell Egg Cholesterol Using Nutritional Approaches

An issue addressed here regards shell egg cholesterol content with histidine feeding as a nutraceutical is in regards to affecting production parameters for egg laying composition, egg size and egg number or rate of production over days.  The modeling of shell egg content and cholesterol metabolism will in the shell egg yolk sac be investigated with respect to the esterification of cholesterol. Cholesterol esterase activity as cholesterol enters the yolk sac is located in the yolk sac membrane (Shand, West, McCartney and Speake, 1993) and with retention or storage of cholesterol in the shell egg, with transgenic manipulating, should be investigated.  Whether there is a "restraining" effect in regards to the interaction between increased egg number and dietary protein treatment on shell egg content related due to cholesterol esterase's function or mechanism remains to be seen.  The prospect of using transgenesis down-regulated expression via gene editing (GE) with transcription engineering for cholesterol esterase could have a limitation to shell egg cholesterol content.

The outlook here is to view research at this point for using histidine to mitigate nutritional demands in production and legitimizing the regulatory need for transgenesis in livestock breeding and which will require further product labelling with use of DNAase on the shell egg product, perceived by the consumer to possess only a negligible rec-DNA contamination. These products include flash-frozen eggs and egg powder.

References

Elkin, R. G. 2006. Reducing Shell Egg Cholesterol Content. I. Overview, Genetic Approaches and Nutritional Strategies. World Poultry Science Journal, 62, 665.

Elkin, R. G. 2007. Reducing Shell Egg Cholesterol Content. II. Review of Approaches Utilizing Non-nutritive Dietary Factors or Pharmacological Agents and An Examination of Emerging Strategies. World Poultry Science Journal, 63, 5.

Elkin, R. G., Bauer, R. and Schneider, W. J. 2012.  Restricted Ovulator Chicken Strain: An Oviparous Vertebrate Model of Reproductive Dysfunction Caused By A Gene Defect Affecting An Oocyte-Specific Receptor. Animal Reproduction Sciences, 136, 1.

Heindrich, J. E., Canlos, L. M., Hunsaker, L. A., Deck, L. M. and Jagt, D. L. V. 2004.  Inhibition of Pancreatic Cholesterol Esterase Reduced Cholesterol Absorption in the Hamster. Bio Med Central Pharmacology, 4, 5.

Mahrous, M. Y. and El-Dlebshany, A. E. M. 2011. Reduction of the Cholesterol Content of Eggs by Introducing Naked Neck (Na) and Frizzle (F) Genes in Laying Hens.  Egyptian Poultry Sciences, 31, 817.

Meaney, S. 2014. Epigenetic Regulation of Cholesterol Homeostasis. Frontiers in Genetics, 5, 1.

Rowghani, E., Boostani, A. D., Mahmmmodian Fard, H. R. and Frouzani, R. 2007.  Effect of Dietary Fish Meal on Production Performance and Cholesterol Content of Laying Hens. Pakistan Journal of Biological Sciences, 10, 1747.

Shand, J. H., West, D. W., McCartney, R. J. and Speake, B. K. 1993. The Esterification of Cholesterol in the Yolk Sac Membrane of the Chick Embryo. Lipids, 28, 621.