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Hippocampal Dihomo‐γ‐Linolenic Acid Partially Mediates the Relationship Between Serum Lauric Acid and Hippocampal Choline Metabolites in the Young Pig
Author(s) -
Mudd Austin T,
Waworuntu Rosaline V,
Berg Brian M,
Donovan Sharon M,
Dilger Ryan N
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.141.6
Subject(s) - hippocampal formation , chemistry , metabolite , fatty acid , choline , endocrinology , phosphocholine , medicine , hippocampus , phospholipid , biochemistry , biology , phosphatidylcholine , membrane
Fatty acids are pivotal for growth and development of the neonate, and the brain is especially susceptible to their presence or absence. There is interest in understanding the mechanisms by which specific fatty acids in the circulation influence development, but relatively little research has explored medium chain fatty acids (MCFA) in this context. Therefore, the objective of this exploratory study was to identify novel relationships whereby circulating MCFA levels modulate hippocampal metabolites. Beginning at 2 d and continuing until 30 d of age, 24 vaginally‐derived male piglets were provided custom milk replacer formulated to meet piglet nutrient requirements. At 30 d of age, piglets underwent magnetic resonance spectroscopy (MRS) procedures to quantify metabolite concentrations in the hippocampus. Following MRS, samples from the right hippocampus and serum were harvested from pigs at 31 d of age for lipidomic profiling. Linear regressions were used to assess the relationship between serum MCFA and hippocampal MRS metabolites, as well as between serum MCFA and hippocampal FA. Subsequently, a mediation model was used to investigate whether the relationships between serum MCFA and hippocampal MRS metabolites were mediated by hippocampal FA. The mediation analysis revealed that hippocampal free dihomo‐γ‐linolenic acid (FA‐20:3n6) partially mediated the relationship between serum free lauric acid (FA‐12:0) and brain glycerophosphocholine plus phosphocholine (GPC‐PCh). First, increased levels of serum FA‐12:0 related to decreased levels of hippocampal FA‐20:3n6 (P = 0.011). Second, increased levels of serum FA‐12:0 related to decreased brain GPC‐PCh (P = 0.002). We observed a significant (P < 0.05; 95% CI: −0.245 to −0.019) indirect path of the mediation (i.e., effect of serum FA‐12:0 though hippocampal FA‐20:3n6 on brain GPC‐PCh). Additionally, the direct path (i.e., effect of serum FA‐12:0 on brain GPC‐PCh, accounting for hippocampal FA‐20:3n6) was also significant (P < 0.05; 95% CI: −0.435 to −0.012). Therefore, hippocampal FA‐20:3n6 partially mediated the relationship between serum FA‐12:0 and brain GPC‐PCh. Overall, these results suggest the levels of circulating FA‐12:0 may be related to hippocampal metabolism of previously unrelated complex lipid moieties. Future research should test for direct effects of altering circulating FA‐12:0 on these metabolites and associated roles in brain development and functions. Support or Funding Information This project was funded by Mead Johnson Nutrition.