Ph D Thesis Amelie Deglaire - TEL

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suggest a higher urea entry in the gut, and possibly a higher faecal excretion, with low-
quality protein than with high-quality protein.
In addition, the level of urease activity in the gut can be influenced by dietary
components. Feeding diets containing high levels of lactose or cellulose has been shown
to reduce urease activity and net ammonia production in the rat intestine (Kim et al.,
1998).
1.6. Large intestine
The large intestine, which comprised the caecum (for rats and pigs only), colon and
rectum, has been reported to secrete 1.6−4.5 g endogenous N/d (Krawielitzki et al., 1994;
Krawielitzki et al., 1996). Microbial N was reported to contribute up to 60−80% of total
faecal N (Stephen & Cummings, 1980; Low & Zebrowska, 1989). However, whereas
microbial activity is maximal in the large intestine, it is also present to a lesser extent in
the duodenum and jejunum, and to an intermediate extent in the ileum (Bach Knudsen et
al., 1991). Bacteria can metabolize N from non-protein (ammonia) or protein sources
from endogenous or dietary origin. Although this measure was undertaken at the ileal
level, an increased dietary protein intake was shown to induce a higher intestinal flow of
bacterial N, mostly due to a higher incorporation of dietary N into microbial proteins
(Bartelt et al., 1999). Fibres have also been reported to enhance intestinal microbial
protein flow (Bartelt et al., 1999; Libao-Mercado et al., 2007).
Intestinal microflora may synthesize de novo IAA. Synthesis and utilization of microbial
IAA have been demonstrated in various monogastric mammals (Niiyama et al., 1979;
Torrallardona et al., 1996; Metges et al., 1999a; Millward et al., 2000b; Backes et al.,
2002; Torrallardona et al., 2003a; Belenguer et al., 2005). Their site of synthesis and
absorption might not be confined to the large intestine and could occur in part in the
small intestine (Torrallardona et al., 2003b). Furthermore, their net contribution to the
AA homeostasis of the host is still being debated (Fuller & Reeds, 1998; Baker, 2005;
Metges & Petzke, 2005; Stoll & Burrin, 2006; Tomé & Bos, 2007; Blachier et al., 2007).
According to Torrallardona et al. (2003a), lysine, and more generally IAA synthesized by
the gastrointestinal microflora, would significantly contribute to fulfil the metabolic IAA
requirements in pigs. However, microbially derived lysine may also be seen as part of the
recycling that occurs for endogenous N and IAA rather than as a net source of AA
supplied in the diet (Metges et al., 1999a; Metges & Petzke, 2005). An important aspect