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CHAPTER 5.2<br />

prepartum period. At the onset <strong>of</strong> lactation, most likely due to formation <strong>of</strong> eicosanoid<br />

products <strong>of</strong> the prostagl<strong>and</strong>in series (Guilbault et al., 1984), the animals in the SHORT<br />

<strong>and</strong> CON group similarly decrease in 20:4n-6 in all blood fractions which was<br />

subsequently mirrored in FF <strong>and</strong> MF during the first 2 weeks <strong>of</strong> lactation. The response<br />

lag up to 2 weeks <strong>of</strong> 20:4n-6 supplementation to appear in BP for LONG has been<br />

reported in humans for 20:5n-3 as well (Cartwright et al., 1985; S<strong>and</strong>ers <strong>and</strong> Hinds,<br />

1992). Overall BP 20:4n-6 remained higher compared with SHORT <strong>and</strong> CON, but despite<br />

continuous dietary supplementation, gradually decreased from week 1 to 2 in lactation.<br />

In contrast, switching to n-3 at 14 DIM, immediately increased 18:3n-3<br />

concentration two-fold in BP, FF <strong>and</strong> MF for SHORT at the end <strong>of</strong> the supplementation<br />

period <strong>and</strong> over a three-fold for the 22:6n-3 in BP, FF <strong>and</strong> MF for LONG. Peripartal<br />

supplementation up to 92 g/kg DM <strong>of</strong> extruded flaxseed increased 5.3-fold in BP, 5.1-<br />

fold in MF (Zachut et al., 2010a) <strong>and</strong> 8.1-fold in FF collected at 63 <strong>and</strong> 96 DIM (Zachut et<br />

al., 2011). Flaxseed, after various treatments (Mustafa et al., 2003; Petit et al., 2004;<br />

Gonthier et al., 2005) provoked similar changes in BP as observed in our study. Also, in<br />

more established lactation (114 DIM), similar results were obtained for BP <strong>and</strong> FF when<br />

feeding extruded flaxseed at dietary inclusion rate <strong>of</strong> 38 g/kg DM, but increases in MF<br />

18:3n-3 were smaller (6.6-fold increase; Zachut et al., 2010b). From our results it can be<br />

concluded that feeding smaller amounts <strong>of</strong> 18:3n-3 is primarily reflected in the 18:3n-3<br />

content in TAG. As the latter fraction is a major source <strong>of</strong> milk FA (Bauman <strong>and</strong> Griinari,<br />

2003), this might explain the faster response in 18:3n-3 MF before changes are observed<br />

in BP <strong>and</strong> FF when feeding smaller amounts <strong>of</strong> flaxseed (Zachut et al., 2010b). In<br />

contrast, a clear TAG enrichment seems to occur for 22:6n-3 when fed at lower rates,<br />

possibly explaining the 3-fold increase in MF compared with a 2-fold for 18:3n-3.<br />

Furthermore, Offer et al. (2001) proved this enrichment to primarily occur in CE, NEFA<br />

<strong>and</strong> PL fraction in high-density lipoproteins (HDL), <strong>and</strong> TAG <strong>and</strong> PL in low-density<br />

lipoproteins (LDL) but not the very low-density lipoproteins (VLDL). Mammary<br />

lipoprotein lipase primarily affects the TAG fraction <strong>of</strong> chylomicrons <strong>and</strong> VLDL to obtain<br />

FA for MF synthesis (Palmquist <strong>and</strong> Mattos, 1978; Moore <strong>and</strong> Christie, 1979; Barber et<br />

al., 1997) explaining the low concentration <strong>of</strong> 22:6n-3 in MF compared to BP <strong>and</strong> FF.<br />

Compared to earlier work, we fed less than 20 g <strong>of</strong> 22:6n-3 as opposed to studies<br />

supplementing over 40 g per day <strong>of</strong> 22:6n-3 with concomitant 10 times higher 22:6n-3<br />

concentration in MF (Boeckaert et al., 2008; Hostens et al., 2011). Limited research has<br />

184

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