Marine lipids
Similar results were obtained by the analysis of docosahexaenoate
balance. Indeed, out of the 1093.7 ± 55.4 mg of ingested 22:6 (n-3),
4.9 ± 1.2 mg were excreted, 329.2 ± 63.4 mg accumulated as 22:6 (n-3)
and 73.3 ± 22.3 mg were retroconverted into 20:3 (n-3) and 22:3 (n-3)
(table 2). In proportion to the 22:6 (n-3) intake, these amounts corresponded to 0.5% , 30.1% and 6.9% (3.8% for 20:5 (n-3) and 3.1% for
22:5 (n-3) respectively for excretion, accumulation and retroconversion.
Therefore 22:6 (n-3) disappearance was 62.5% (± 7.0). Concerning the
specific accumulation of 22:6 (n-3), 68.2%, were deposited m the
remaining carcass (224.4 ± 35.3 mg), 16.8(7 in total fat(35.0 ± 20.6 mg
in internal fat and 20.6 ± 17.5 mg in subcutaneous fat), 9-9% in liver
(32.7 ± 8.3 mg) and 1.1% in brain (3.7 ± 0.7 mg) corresponding to
the same content as in group "18:3 (n-3)" (fig. B).
Discussion
The main result of the present study is that the apparent β-oxidation
rate of 22:6 (n-3) was similar to that of 18:3 (n-3) (62.5% versus 59%).
Therefore, for both fatty acids, whole bocly (n-3) fatty acid accumulation
was around 40 per cent. The 18:3 (n-3) was mainly deposited in total fat
(50% of total 18:3 (n-3) and 22:6 (n-3) in the remaining carcass (70%).
The 18:3 (n-3) used to be considered as actively involved in the energy
metabolism due to its high β-oxidation rate and storage in total fat.
Indeed, the β-oxidation rate of 18:3 (n-3) in vivo was measured to be
around 75% using tracer studies in the rat (Leyton et al., 1987) and rose
up to 85% for apparent β-oxidation using the balance fatty acid method
in the growing rat (Cunnane & Anderson, 1997). However, in the latter
study, animals received a 10 weight % fat diet providing 920 mg
18:3 (n-3) per 100 g diet. This 18:3 (n-3) supply was five-fold higher than
the (n-3) fatty acid requirement of the growing rat (200 mg 18:3 (n-3)
per 100 g of diet i.e. 0.45% of total dietary energy) (Guesnet et al., 1997).
Using the same methodology but a 5 weight % fat diet providing the
minimal requirement in 18:3 (n-3), we found here a significantly lower
apparent β-oxidation rate (60% versus 85%). Moreover, 18:3 (n-3)
storage in total fat was also lower (50% versus 79%). Interestingly, we
observed a similar quantitative deposition of desaturation-elongation
products (i.e. 20:5 (n-3), 22:5 (n-3) and 22:6 (n-3) with about 200220 milligrammes. We concluded that, given the dietary content of total
lipids and/or 18:3 (n-3), the organism adapted to both of the |3-oxidation and the deposition rate of the 18:3 (n-3) in aclipose tissue in order
to lead to an optimal whole body deposition of (n-3) long-chain fatty
acids. Therefore, higher dietary content of total lipids and/or 18:3 (n-3)
would lead to a higher β-oxidation rate of 18:3 (n-3).
The in vivo β-oxidation rate of 22:6 (n-3) found in our study (62.5% of
apparent β-oxidation) has no direct comparison in the literature. In vitro,
only few studies have been conducted on the β-oxidation of 22:6 (n-3);
although 22:6 (n-3) is a poor substrate for both mitochondrial and
160
Similar results were obtained by the analysis of docosahexaenoate
balance. Indeed, out of the 1093.7 ± 55.4 mg of ingested 22:6 (n-3),
4.9 ± 1.2 mg were excreted, 329.2 ± 63.4 mg accumulated as 22:6 (n-3)
and 73.3 ± 22.3 mg were retroconverted into 20:3 (n-3) and 22:3 (n-3)
(table 2). In proportion to the 22:6 (n-3) intake, these amounts corresponded to 0.5% , 30.1% and 6.9% (3.8% for 20:5 (n-3) and 3.1% for
22:5 (n-3) respectively for excretion, accumulation and retroconversion.
Therefore 22:6 (n-3) disappearance was 62.5% (± 7.0). Concerning the
specific accumulation of 22:6 (n-3), 68.2%, were deposited m the
remaining carcass (224.4 ± 35.3 mg), 16.8(7 in total fat(35.0 ± 20.6 mg
in internal fat and 20.6 ± 17.5 mg in subcutaneous fat), 9-9% in liver
(32.7 ± 8.3 mg) and 1.1% in brain (3.7 ± 0.7 mg) corresponding to
the same content as in group "18:3 (n-3)" (fig. B).
Discussion
The main result of the present study is that the apparent β-oxidation
rate of 22:6 (n-3) was similar to that of 18:3 (n-3) (62.5% versus 59%).
Therefore, for both fatty acids, whole bocly (n-3) fatty acid accumulation
was around 40 per cent. The 18:3 (n-3) was mainly deposited in total fat
(50% of total 18:3 (n-3) and 22:6 (n-3) in the remaining carcass (70%).
The 18:3 (n-3) used to be considered as actively involved in the energy
metabolism due to its high β-oxidation rate and storage in total fat.
Indeed, the β-oxidation rate of 18:3 (n-3) in vivo was measured to be
around 75% using tracer studies in the rat (Leyton et al., 1987) and rose
up to 85% for apparent β-oxidation using the balance fatty acid method
in the growing rat (Cunnane & Anderson, 1997). However, in the latter
study, animals received a 10 weight % fat diet providing 920 mg
18:3 (n-3) per 100 g diet. This 18:3 (n-3) supply was five-fold higher than
the (n-3) fatty acid requirement of the growing rat (200 mg 18:3 (n-3)
per 100 g of diet i.e. 0.45% of total dietary energy) (Guesnet et al., 1997).
Using the same methodology but a 5 weight % fat diet providing the
minimal requirement in 18:3 (n-3), we found here a significantly lower
apparent β-oxidation rate (60% versus 85%). Moreover, 18:3 (n-3)
storage in total fat was also lower (50% versus 79%). Interestingly, we
observed a similar quantitative deposition of desaturation-elongation
products (i.e. 20:5 (n-3), 22:5 (n-3) and 22:6 (n-3) with about 200220 milligrammes. We concluded that, given the dietary content of total
lipids and/or 18:3 (n-3), the organism adapted to both of the |3-oxidation and the deposition rate of the 18:3 (n-3) in aclipose tissue in order
to lead to an optimal whole body deposition of (n-3) long-chain fatty
acids. Therefore, higher dietary content of total lipids and/or 18:3 (n-3)
would lead to a higher β-oxidation rate of 18:3 (n-3).
The in vivo β-oxidation rate of 22:6 (n-3) found in our study (62.5% of
apparent β-oxidation) has no direct comparison in the literature. In vitro,
only few studies have been conducted on the β-oxidation of 22:6 (n-3);
although 22:6 (n-3) is a poor substrate for both mitochondrial and
160