Duodenal and Milk Trans Octadecenoic Acid and Conjugated Linoleic Acid (CLA) Isomers Indicate that Postabsorptive Synthesis Is the Predominant Source of cis-9-Containing CLA in Lactating Dairy Cows

Abstract

Duodenal and milk samples obtained from lactating cows in a previous study were analyzed to compare the content and isomer distribution of conjugated linoleic acids (CLA) and trans-18:1 fatty acids (tFA). Four diets containing either low [25 g/100 g dry matter (DM)] or high (60 g/100 g DM) forage were fed with or without 2% added buffer to four multiparous Holstein dairy cows in a 2 x 2 factorial, 4 x 4 Latin square design with 3-wk experimental periods. Duodenal flows of CLA were low (1.02-1.84 g/d), compared with that of tFA (57-120 g/d), regardless of diet. The greatest amounts of CLA and tFA, as well as the greatest proportions of trans-10-18:1 (P < 0.02), and cis-9, trans-11 (P < 0.01) and trans-10, cis-12 CLA (P < 0.01) were in the duodenal flow of cows fed the low forage unbuffered diet. In milk fat, tFA were increased by the low forage unbuffered diet and the trans-10-18:1 (P < 0.02) replaced trans-11-18:1 as the major 18:1 isomer. Milk CLA secretion (7.2-9.1 g/d) was greater (P < 0.001) than that in the duodenal flow with each diet. This was due to the increase in cis-9, trans-11-18:2 and trans-7, cis-9 CLA, resulting most likely from endogenous synthesis via Delta9-desaturation of ruminally derived tFA. For other CLA isomers, duodenal flow was always greater than milk secretion, suggesting that they essentially were produced in the rumen.

Production of trans C18:1 and conjugated linoleic acid in continuous culture fermenters fed diets containing fish oil and sunflower oil with decreasing levels of forage

“…The linear increase in trans C18:1 concentration indicates that low ruminal pH favours trans C18:1 accumulation. Low ruminal pH, caused by a high-concentrate diet, increased the accumulation of trans C18:1 in other studies (Karlscheur et al, 1997;Piperova et al, 2002;Loor et al, 2004b). Although this study and others (Karlscheur et al, 1997;Piperova et al, 2002;Loor et al, 2004b) clearly show that low rumen pH promotes trans C18:1 accumulation, the mechanism is still unknown.…”

“…Low ruminal pH, caused by a high-concentrate diet, increased the accumulation of trans C18:1 in other studies (Karlscheur et al, 1997;Piperova et al, 2002;Loor et al, 2004b). Although this study and others (Karlscheur et al, 1997;Piperova et al, 2002;Loor et al, 2004b) clearly show that low rumen pH promotes trans C18:1 accumulation, the mechanism is still unknown. The accumulation of trans C18:1 under low rumen pH conditions may be caused by altering the rumen ecosystem and/or inhibiting the reductase activity of ruminal microorganisms, causing the accumulation of trans C18:1.…”

“…Formation of trans C18:1 and CLA in the rumen are influenced by dietary supplementation with unsaturated vegetable oils (AbuGhazaleh et al, 2003;Loor et al, 2004a and b) or changes in rumen pH as a result of alterations in dietary forage to concentrate ratios (F:C) (Piperova et al, 2002;Loor et al, 2003;Sackmann et al, 2003).…”

“…Studies examining the effect of forage or concentrate feeding on the distribution of trans C18:1 and CLA isomers in the rumen (Loor et al, 2004a) or ruminant fat (Sackmann et al, 2003;Aharoni et al, 2004;Loor et al, 2005) have used only vegetable oils or FO. Feeding high concentrate diets (Piperova et al, 2002) or low forage diets supplemented with vegetable oils rich in linoleic acid or FO (Loor et al, 2004a) altered ruminal biohydrogenation resulting in t10 rather than VA being the predominant trans C18:1 intermediate. Alterations in the profile of trans C18:1 intermediates formed in the rumen have direct consequences on the supply of VA available for endogenous conversion in the mammary gland into c9t11 CLA .…”

Conjugated linolenic acid (CLnA), conjugated linoleic acid (CLA) and other biohydrogenation intermediates in plasma and milk fat of cows fed raw or extruded linseed

“…In our experiment, with diet C, the trans-13 1 14 18:1 proportion was 66% and 55% of that of trans-10 1 11 18:1 in plasma and milk, respectively, and proportions of trans-12 18:1, trans-15 18:1, and trans-16 18:1 were all around 10% of the total trans-18:1 in plasma and milk. Trans-12 18:1, trans-15 18:1, and trans-16 18:1 have already been suggested to be produced during cis-9, cis-12 18:2 BH (Loor et al, 2002), in addition to their production during cis-9 18:1 (Mosley et al, 2002) and cis-9, cis-12, cis-15 18:3 BH, and Piperova et al (2002) published a distribution of trans-18:1 isomers close to ours in the milk from cows fed a diet without added fat, and where cis-9, cis-12, cis-15 18:3 represented 10.8% of the total dietary FA. On the contrary, Loor et al (2005) found, with a diet without added fat but where cis-9, cis-12, cis-15 18:3 represented 25.8% of the total dietary FA, that trans-13 1 14 18:1 proportion was only 24% of that of trans-10 1 11 18:1 in milk, but 61% in plasma.…”