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Concentration of milk free fatty acids is increased during lactational mastitis
Author(s) -
Hunt Katherine Mary,
Williams Janet E,
Hunt Martha K,
Ting Robert,
Behre Rebecca,
McGuire Michelle K,
Shafii Bahman,
McGuire Mark A
Publication year - 2010
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.24.1_supplement.556.21
Subject(s) - mastitis , lactation , lipolysis , fatty acid , lauric acid , breast milk , oleic acid , chemistry , milk fat , food science , zoology , medicine , biology , biochemistry , adipose tissue , pregnancy , microbiology and biotechnology , genetics , linseed oil
Free fatty acids (FFA) are minor constituents of human milk lipids, but may have important antibacterial properties. The objective of this study was to investigate whether lactational mastitis alters the total lipid (TL), FFA, and phospholipid (PL) contents of human milk. Participants ( n = 13) were women with diagnosed mastitis referred to us by physicians and lactation consultants. Complete breast expressions were collected from infected and non‐infected breasts, with the healthy milk of each sample pair serving as the control. TL was extracted from each sample and fractionated using solid phase extraction. TL, FFA, and PL were then converted into methyl esters and analyzed by gas chromatography. Statistical analysis was performed using the Wilcoxon Signed‐Rank Test. There was no difference in the fatty acid profiles or overall amounts of TL and PL. However, percent FFA was greater ( P = 0.0007) in infected milk compared with the non‐infected milk (1.33 ± 0.195 vs 1.07 ± 0.122%, respectively). This was accompanied by minor changes in the fatty acid profile of the FFA fraction with a decrease ( P < 0.05) in lauric acid (12:0) and an increase in α‐linolenic acid (18:3ω3) in infected milk. This increase in FFA and the lack of change in TL indicate the potential role of increased lipolysis during mastitis as either a promoter of or response to inflammation. Supported by NIH‐NRRI grant P20 RR15587. Grant Funding Source : NIH‐NRRI grant P20 RR15587