Dose effect of α‐linolenic acid on PUFA conversion, bioavailability, and storage in the hamster

Abstract

If an increased consumption of alpha-linolenic acid (ALA) is to be promoted in parallel with that of n-3 long-chain-rich food, it is necessary to consider to what extent dietary ALA can be absorbed, transported, stored, and converted into long-chain derivatives. We investigated these processes in male hamsters, over a broad range of supply as linseed oil (0.37, 3.5, 6.9, and 14.6% energy). Linoleic acid (LA) was kept constant (8.5% energy), and the LA/ALA ratio was varied from 22.5 to 0.6. The apparent absorption of individual FA was very high (>96%), and that of ALA remained almost maximum even at the largest supply (99.5%). The capacity for ALA transport and storage had no limitation over the chosen range of dietary intake. Indeed, ALA intake was significantly correlated with ALA level not only in cholesteryl esters (from 0.3 to 9.7% of total FA) but also in plasma phospholipids and red blood cells (RBC), which makes blood components extremely reliable as biomarkers of ALA consumption. Similarly, ALA storage in adipose tissue increased from 0.85 to 14% of total FA and was highly correlated with ALA intake. As for bioconversion, dietary ALA failed to increase 22:6n-3, decreased 20:4n-6, and efficiently increased 20:5n-3 (EPA) in RBC and cardiomyocytes. EPA accumulation did not tend to plateau, in accordance with identical activities of delta5- and delta6-desaturases in all groups. Dietary supply of ALA was therefore a very efficient means of improving the 20:4n-6 to 20:5n-3 balance.

Dose effect of alpha-linolenic acid on lipid metabolism in the hamster

“…Under these conditions, the only variable was the oleic/ALA ratio, and a previous study showed that ALA transport, storage, and conversion into EPA were strictly proportional to dietary ALA intake (30). By contrast, in the present study, increasing dietary ALA did not result in a linear dose-response of all lipid parameters that were affected in different ways: (i) plasma TG and cholesterol responded to the lowest ALA supply (10% FA, 3.6% total energy) and were not further affected by higher doses; (ii) the activity of lipogenic enzymes (ACC and ME) was negatively correlated to dietary ALA intake; (iii) liver TC, faecal excretion of TC and BA, and BA profiles varied only with very high ALA intakes.…”

“…Fatty acid methyl esters (FAME) were analysed by GLC with a chromatograph (Fisons 8000, Thermo products, Les Ulis, France) under the conditions described by Morise et al [30]. Saponification of lipids was performed at 85 °C with ammonia (2 N) in ethanol, then neutral sterols (containing cholesterol and phytosterols) were extracted with petroleum ether, using 14 Ccholesterol (Perkin Elmer Life Sciences, Boston, USA, 45 mCi·mmol -1 ) as a marker.…”

“…Besides, under the same nutritional conditions, both ALA and EPA were transported and stored proportionally to dietary ALA intake [30]. Therefore, it remains difficult to decide which fatty acid is the most potent inhibitor of lipogenesis in vivo.…”

“…We chose the hamster as a validated model for assessing the effects of dietary fats on lipid metabolism [27][28][29]. Moreover, our previous study in this model demonstrated that PUFA conversion, bioavailability and storage in the hamster is highly responsive to the dietary dose of ALA [30]. Indeed, ALA transport in plasma cholesteryl esters (CE) and storage in adipose tissue, as well as conversion into EPA (as assessed by the EPA proportion in phospholipids (PL) from plasma, red blood cells and the heart) were proportional to the dietary ALA dose, and did not tend to a plateau.…”

“…Under the same nutritional conditions, ALA transport, storage and conversion into EPA was shown to be strictly proportional to dietary intake [30]. This linear relationship has to be taken into account in discussing the dose effect of dietary ALA on lipid metabolism.…”