|ZACEK, PETR - Us Forest Service (FS)|
|JOHNSON, LUANN - University Of North Dakota|
Submitted to: Keystone Symposia
Publication Type: Abstract Only
Publication Acceptance Date: 12/1/2016
Publication Date: 2/1/2017
Citation: Zacek, P., Bukowski, M.R., Idso, J.P., Johnson, L., Picklo, M.J. 2017. Dietary saturated fatty acid type modifies the plasma phospholipidome in obese mice [abstract]. Keystone Symposia. p.50.
Technical Abstract: A high intake of saturated fatty acids (SFA) is associated with obesity and its related diseases. However, the contribution of particular SFAs to obesity has not been investigated. We tested the hypothesis that the composition of dietary SFA causes selective changes in the plasma phospholipidome in obese mice. Male, C57/Bl6 mice were fed obesogenic diets of 48% energy (en) fat (28% SFA, 14% oleic acid, and 6% polyunsaturated fatty acid) or a control diet with 16% en fat (5% SFA, 4% oleic acid, and 7% PUFA) for 16 weeks. Obesogenic groups were divided by SFA source: coconut oil-based (CNO) with high lauric acid, a palm-oil based (PO) with palmitic acid and stearic acids, and a MIX group with similar levels of the SFAs. All mice eating the obesogenic diets became obese compared to the control group. Hepatic lipids were elevated in the PO and MIX groups, but not the CNO group. While all obese animals were insulin resistant, PO animals had higher insulin resistance than CNO and MIX animals. Plasma phosphatidylcholine (PC) and phosphatidylethanolamine (PE) species were analyzed by an infusion-based shotgun MS/MS method. We quantified 53 PE and 122 PC species. Obesity-dependent and SFA-type dependent changes in PE and PC species were observed. Intake of the PO diet increased the content of several plasma PCs containing arachidonic acid and docosahexaenoic acid. Principal component analysis of the phospholipidomic data demonstrated a separation of all four different dietary groups. Our data demonstrate that eating an obesogenic diet induced some lipidomic changes independent of SFA type, but that SFA-specific lipidomic changes were present that were concomitant with hepatic lipid accumulation and insulin resistance.