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GENERAL DISCUSSION<br />

DISTRIBUTION OR REDISTRIBUTION OF FATTY ACIDS TO THE REPRODUCTIVE<br />

TRACT<br />

One <strong>of</strong> the most trivial processes when evaluating the link between the<br />

metabolism <strong>and</strong> the ovarian compartment, especially when evaluating the effect <strong>of</strong> FA, is<br />

the physical barrier between the blood <strong>and</strong> the follicular cavity which serves as an<br />

avascular compartment in which the oocyte is subdued to a highly orchestrated process<br />

<strong>of</strong> growth, prematuration <strong>and</strong> maturation (Picton et al., 2008; Ferreira et al., 2009). The<br />

pathway via which FA intervene in these processes is partly mediated in the way they<br />

are being released into the bloodstream, transported to <strong>and</strong> subsequently are taken up<br />

by e.g. the ovary, but experiments in this research area are rare.<br />

During lipolysis, TAG catabolism is initiated by adipose tissue lipases which<br />

transform the insoluble TAG into NEFA which are released via FA transfer proteins<br />

(FATP) <strong>and</strong> FA translocase (FAT) into the blood (Bionaz <strong>and</strong> Loor, 2008; Contreras <strong>and</strong><br />

Sordillo, 2011; Figure 4). Typically, NEFA are bound to albumin, although a very small<br />

portion can be transported as unbound monomers in aqueous solution (Richieri <strong>and</strong><br />

Kleinfeld, 1995). The follicular wall has been documented to be permeable via<br />

paracellular transport for molecules such as albumin <strong>and</strong> other proteins (Edwards, 1974;<br />

Gosden et al., 1988). In Chapters 5.1 <strong>and</strong> 5.2, albumin concentration did not differ<br />

between plasma <strong>and</strong> FF, which implies differences in NEFA concentrations cannot be<br />

attributed to differences in the concentration <strong>of</strong> their carrier molecule. The higher NEFA<br />

in plasma compared to the FF, as in our (Chapters 5.1 <strong>and</strong> 5.2) <strong>and</strong> other studies (Leroy<br />

et al., 2005; Shehab-El-Deen et al., 2010), has been explained by Chung et al. (1995) by a<br />

substantial partitioning <strong>of</strong> NEFA into low density lipoproteins (LDL) in case <strong>of</strong> excessive<br />

plasma NEFA concentrations. Interestingly in the same study, the partitioning <strong>of</strong> FA was<br />

shown to be ‘saturation dependent’ with saturated FA mainly being partitioned to the<br />

LDL whereas unsaturated FA remained albumin bound (Chung et al., 1995). The latter<br />

might explain the higher PUFA content which has been observed in NEFA FF when<br />

compared to plasma (Moallem et al., 1999; Leroy et al., 2005; Renaville et al., 2010).<br />

248

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