9:00 am - 10:00 am
A graduate exam seminar is a presentation of the student’s final research project for their degree.
This is an ALES PhD Final Exam Seminar by Paulina Aldana Hernández. This seminar is open to the general public to attend.
https://ualberta-ca.zoom.us/j/97460725796?pwd=aXpuR1FOWURyV0ZUWlAyZkYwYVcwUT09
Meeting ID: 974 6072 5796
Passcode: 856675
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Meeting ID: 974 6072 5796
Passcode: 856675
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Thesis Topic: The role of dietary choline on atherosclerosis development
PhD with Dr. René Jacobs.
Seminar Abstract:
Choline, an essential nutrient, is needed for a variety of biological processes such as phospholipid synthesis, cell-membrane signaling, lipoprotein secretion, acetylcholine biosynthesis, and one-carbon metabolism. In the North American diet, the two most common forms of choline in foods are phosphatidylcholine (PC) and free-choline (FC). During the last decade epidemiological studies have suggested that consumption of choline-rich foods (specifically PC from animal source) might increase cardiovascular disease (CVD) risk. Excess dietary choline is metabolized by gut microorganisms to trimethylamine (TMA) and then is further oxidized in the liver to form trimethylamine N-oxide (TMAO). It has been proposed that TMAO might enhance atherosclerosis development and be a biomarker for CVD risk. Therefore, the objective of this thesis was to understand the role of dietary choline supplementation on atherosclerosis development.
A series of feeding trials were conducted to investigate whether the form of dietary choline, FC or PC supplementation influences atherosclerosis development in atherogenic mouse models. In Ldlr-/- mice, dietary supplementation with 10X FC or TMAO increased plasma TMAO levels (1.6- and 4-fold, respectively) after 8 wk. After 16 wk there was an increase of 2-fold at TMAO supplementation. In Apoe-/- mice. However, following the dietary intervention for 28 wk in this mouse model, TMAO levels were significantly (p<0.05) increased in FC and TMAO groups compared to controls, 1.8 and 1.5-fold respectively. These dietary interventions did not alter atherosclerosis or plasma cholesterol levels in either mouse model.
To our surprise, PC supplementation (4X of total choline) reduced atherosclerotic lesions (p<0.05) while increasing (2-fold higher) plasma TMAO levels in Ldlr-/- mice. In the fasting state, PC supplementation decreased plasma VLDL-C and APOB48, and increased plasma HDL-C. However, VLDL secretion was not affected by dietary treatment. We observed lower (p<0.05) levels of circulating pro-atherogenic chemokines in the PC supplemented group. This study suggests that increased dietary PC intake protects against atherosclerosis.
While dietary choline and PC supplementation increase plasma TMAO levels, our studies did not find a causative relationship between dietary choline and atherosclerosis. Our studies also suggest that consumption of dietary PC may reduce the development of CVD risk.
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