Date of Graduation


Document Type


Degree Type



Davis College of Agriculture, Natural Resources and Design


Animal and Nutritional Sciences

Committee Chair

Janet Tou

Committee Co-Chair

Vagner Benedito

Committee Member

Jianbo Yao


Omega-3 polyunsaturated fatty acid (n-3 PUFA) consumption has increased through diet and supplementation due to reports of health benefits. The objective of this study was to determine whether different n-3 PUFA sources play a role in lipid metabolism by altering lipogenic gene expression, serum lipids and lipoproteins, and inflammation. Young (aged 28 days) female Sprague-Dawley rats were assigned to one of six diets: corn oil (CO, control), flaxseed oil (FO), krill oil (KO), menhaden oil (MO), salmon oil (SO), or tuna oil (TO). qPCR was used to analyze relative gene expression. Only MO-fed rats had down-regulated gene expression of the lipogenic transcription factor sterol regulatory element binding protein 1c (SREBP-1c) (P=0.007), and downstream enzymes, fatty acid synthase (FAS) (P=0.001) and stearoyl coenzyme A desaturase 1(SCD-1) (P=0.008). MO-fed rats had lower (P<0.001) hepatic arachidonic acid (ARA) content compared to rats fed SO, TO, and CO. Rats fed all n-3 PUFA sources had down-regulated FAS gene expression, except KO. There were no significant changes in expression of lipogenic genes in the hepatic tissue of rats fed KO. Only TO, with the lowest eicosapentaenoic acid:docosahexaenoic acid (EPA:DHA) ratio in hepatic tissue, downregulated SCD-1 gene expression. In the gonadal adipose tissue, FO was the only oil source to alter lipolytic gene expression. PPARgamma was up-regulated in FO (P=0.04) compared to CO-fed rats. FO had the highest (P<0.05) EPA:DHA ratio in gonadal adipose tissue. All n-3 PUFA sources decreased lipogenesis, evidenced by decreased (P<0.05) serum high density lipoprotein (HDL-C), and marine sources of n-3 PUFAs decreased (P<0.05) serum total cholesterol (CHL). Higher dietary 18:1 may be transported to extrahepatic tissues as indicated by the absence of decreased (P>0.05) serum total CHL in FO. All n-3 LC-PUFA sources altered inflammation related hepatic Inhibitor of Kappa B alpha (IKBalpha) gene expression, except the MO group which was the only n-3 PUFA that down-regulated lipogenic transcription factor SREBP-1c. Based on the study results, the MO diet caused a low hepatic ARA content and subsequently affected lipogenic gene expression the most; high EPA and DHA content in the SO and TO diets caused the most decrease in circulating lipids; and all n-3 PUFAs affected gene expression related to inflammation, except for the MO diet group which altered the transcription factor SREBP-1c. Therefore, different sources of n-3 PUFAs had different effects on lipogenesis and lipolysis gene expression which affects lipid metabolism indicated by reduced circulating lipids and lipoproteins, and inflammation which may play a role in cardiovascular disease (CVD) risk.