Krill Oil Addition to 8‐weeks of High‐fat Diet Enhances mTORSer2448 Phosphorylation in Rat Heart

Abstract

Krill oil (KO) derived from shrimp‐like crustaceans, has been marketed as a substantial source of dietary long chain omega‐3 (LC n‐3) polyunsaturated fatty acids, particularly rich in eicosapentaenoic acid (EPA; 20:5 n‐3) and docosahexaenoic acid (DHA; 22:6 n‐3). Consumption of EPA and DHA has been linked to the reduction of cardiovascular disorders including coronary heart disease and myocardial infarction, however the cellular mechanism for these cardioprotective benefits is unclear. The mechanistic target of rapamycin (mTOR) is a Ser/Thr kinase that acts a nutrient sensor, subsequently controlling various key cellular processes including cell growth, cell survival, and protein synthesis. Diets high in saturated fat content have been associated with myocardial dysregulation through alteration of the mTOR signaling pathway, suggesting that interventions that ameliorate mTOR signaling may counter these deleterious effects in the heart. The goal of the current study is to determine the effect of krill oil supplementation to a high saturated fat diet on mTOR signaling in cardiac muscle. Male Sprague‐Dawley rats (approximately 12 months‐old), were assigned by mass to one of three isocaloric dietary groups for 8 weeks: control diet group (CON; 17% saturated fat, 54% carbohydrate, 29% protein; n=8), a high saturated fat group (HF; 42% saturated, 43% carbohydrate, 15% protein; n=12), and a high fat group with krill oil supplementation (KO; 34% saturated fat, 8% krill oil, 43% carbohydrate, 15% protein; n=12). All rats were given ad libitum access to food and water. Body weights and food consumption was recorded weekly. After 8 weeks of dietary intervention and an overnight fast, blood and hearts were collected from anesthetized rats during a terminal surgery. Western immunoblot analysis was used to determine phosphorylation levels of key mTOR signaling proteins including mTORSer2448, p70S6KThr389, 4E‐BP1Thr37/46, eIF4ESer209, and eIF2αSer51. There was no difference in body mass between dietary groups after 8 weeks of treatment. There was a significant increase (p<0.05) in phosphorylation of mTORSer2448 in the KO group when compared to the HF and CON groups. Phosphorylation of downstream targets of mTOR was not different between groups. Eight weeks of KO supplementation can enhance phosphorylation of mTORSer2448, however the cardioprotective impact of this remains unknown. Further research is needed to examine how KO consumption can affect other key downstream mTOR‐related targets associated with improved cardiovascular health.Support or Funding InformationResearch was supported by intramural grants from the College of Health Professions and the Office of Research and Graduate Studies at Central Michigan University.