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CHAPTER 6<br />

records. The UFA content <strong>of</strong> selected herds was 30.8% <strong>and</strong> aligns with literature on milk<br />

UFA (Jensen, 2002; Lock <strong>and</strong> Bauman, 2004). From our data it cannot be concluded<br />

whether a higher UFA content originates from an increase in mono unsaturated FA<br />

(MUFA), poly unsaturated FA (PUFA) or both, which mainly depends <strong>of</strong> the FA pr<strong>of</strong>ile <strong>of</strong><br />

dietary lipids (Chilliard <strong>and</strong> Ferlay, 2004). However, next to PUFA supplementation,<br />

increased UFA in bulk tank milk samples can be explained through other pathways. The<br />

highest proportion <strong>of</strong> UFA in MF is accounted for by 18:1 cis-9 (Jensen, 2002). An<br />

increased concentration in 18:1 cis-9 in MF can originate from both an increased supply<br />

<strong>of</strong> 18:1 cis-9 or its precursor 18:0 to the mammary gl<strong>and</strong> (Glasser et al., 2008). An<br />

increase in 18:1 cis-9 has been associated with increased body fat mobilisation during<br />

ketosis (Van Haelst et al., 2008). However, a contribution <strong>of</strong> FA from lipomobilisation in<br />

cows in positive EBAL to milk FA cannot be excluded, especially for 18:0 <strong>and</strong> 18:1 cis-9<br />

(Chilliard et al., 1991). Furthermore, the induction <strong>of</strong> a MFD has been associated with an<br />

increase in trans-FA <strong>and</strong> proportional decrease in saturated FA increasing the milk UFA<br />

(Griinari et al., 1998; Bauman <strong>and</strong> Griinari, 2003). An increased rumen unsaturated FA<br />

load (RUFAL) has been determined as one <strong>of</strong> the risk factors for a lower FAT content<br />

when accompanied by an altered rumen fermentation (Relling <strong>and</strong> Reynolds, 2007;<br />

Harvatine et al., 2009). The prerequisite <strong>of</strong> both risk factors is mirrored in the significant<br />

but small proportion <strong>of</strong> the variation in FAT explained by UFA in our study (10.2%).<br />

Researchers have focussed on many aspects <strong>of</strong> dairy cow fertility but the<br />

complete biological window in which UFA attenuate fertility is yet to be revealed.<br />

Though small differences were found (IQR max 3 d) which might not be <strong>of</strong> real biological<br />

relevance, we did demonstrate a positive association between DIMFI <strong>and</strong> milk UFA.<br />

However, earlier resumption <strong>of</strong> postpartum cyclicity has not been observed when<br />

feeding FA to dairy cows (Juchem et al., 2010; Silvestre et al., 2011). Interestingly, high<br />

UFA was associated with the highest DIMFI especially when accompanied by a low level<br />

<strong>of</strong> variation, which has to our most recent knowledge not been described. Feeding n-6<br />

UFA to dairy cows has been shown to stimulate PGF2α metabolism improving uterine<br />

health (Petit et al., 2004; Robinson et al., 2002). In contrast, feeding n-3 UFA reduced<br />

endometrial secretion <strong>of</strong> PGF2α, thereby inducing antiluteolytic effects on the corpus<br />

luteum (Staples et al., 1998). These subtle differences between n-6 <strong>and</strong> n-3 FA could<br />

explain differences in DIMFI but cannot be attributed to our study from the parameter<br />

milk UFA which does not distinct between FA.<br />

216

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