| Fats as indicators of physiological constraints in newborn and young reindeer: Rangifer tarandus tarandus L. | ||
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During the first few postnatal weeks when their major feed is milk, newborn ruminants resemble monogastric animals in their digestive physiology and lipid metabolism (Noble 1981). Thereafter, the specialization to the use of poorly digestible vegetation occurs at a rate that varies between species but occurs in most domestic ruminants by the age of 4-6 weeks (Noble 1981). Ruminants are able to disrupt cellulose of low-quality forages by microbial fermentation in anaerobic conditions of rumen or in forestomachs anterior to the true stomachs (Christie 1981). As a result of fermentation, large amounts of volatile fatty acids are synthesized and they, rather than glucose, are the principal sources for lipid synthesis in ruminants (Ballard et al. 1969). The main source of lipid synthesis is acetate and the main sites of lipid synthesis are intestine and adipose tissue, and not the liver as in the non-ruminants (Christie 1981).
Dietary lipids do not directly affect the fatty acid composition of ruminant adipose tissues, as they do in non-ruminants (Christie 1981, Lin et al. 1993, Sarkkinen et al. 1994). Unsaturated fatty acids in the diet are hydrogenated in the rumen, and as a consequence, they are incorporated only in small proportions in adipose tissues that are characterized with a high proportion of saturated fatty acids (Christie 1981, Garton & Duncan 1971, Pond et al. 1993). In addition, the ruminant lipids are synthesized mainly endogenously from the lipid precursors produced by the rumen (Christie 1981). The exception of the low proportion of unsaturated fatty acids in ruminant WAT is the high proportion of unsaturated fatty acids in leg bone marrow (Meng et al. 1969, West & Shaw 1975, Turner 1979, Christie 1981, Pond et al. 1993). Moreover, there are high proportions of PUFAs in two major lipids of blood, cholesteryl esters (CEs), and phospholipids (PLs) in ruminants (Christie 1981, Noble 1981, 1984), Only a small amount of dietary PUFAs are esterified to circulating TAGs, or occur as the FFAs that are both minor lipids in ruminant blood (Noble 1984). The plasma of newborn ruminants contain very low proportions of the principal PUFAs, 18:2 and 18:3n-3, as compared to adult animals (Christie 1981, Noble 1981), obviously resulting from a low supply of these fatty acids during the foetal development (Elphick et al. 1979). Due to the high incorporation of PUFAs in structural lipids, ruminants are believed to withstand low dietary supplies of PUFAs rather well (Noble 1984).
There has been low interest in the fatty acid composition of ruminant adipose tissues as an indicator of nutritional status because they do not seem to clearly respond to dietary changes. There is evidence that unsaturated fatty acids and specific PUFAs are preferentially mobilized from the adipose tissues of non-ruminants such as fasting rodents (Chen et al. 1995) and fasting emperor penguins (Groscolas 1990), and this may be a mechanism for sustaining the PUFA metabolism and its related important functions during undernutrition (Chen & Cunnane 1992, Andriamampandry et al. 1996). In early stages, the decrease in dietary PUFAs in rodents and humans can be seen as significant reductions in the proportions of the principal PUFAs in serum lipids (Chen & Cunnane 1992, Leichsenring et al. 1995). The conditions that strongly decrease the supply of PUFAs - prolonged deprivation of food in particular - could be expected to decrease the proportions of PUFAs in adipose tissues and serum lipids also in ruminants. The availability of lipids and PUFAs in young animals is important, e.g. for cellular growth (Innis 1991, Bruckner 1992), and their deficiency may impair steroid hormone synthesis (Pond 1998). A low supply of lipid precursors and PUFAs may contribute to retarding growth in freely ranging young ruminants during winter. If significant, the reductions in dietary PUFAs can have also other metabolic consequences.