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We report the effect of an atherogenic diet supplemented with cis-9, trans-11-octadecadienoic acid (c9t11), linoleic acid (LA) or an isomeric mixture of conjugated linoleic acids (CLA) on plasma lipids, weight gain and food intake of male Golden Syrian hamsters. Animals were assigned to three diet groups (n = 10), and fed nonpurified diet, supplemented with 10% hydrogenated coconut oil and 0.05% cholesterol for 6 wk. The first diet group was further supplemented with 1% CLA (CLA group), the second diet group with 0.2% c9t11 (c9t11 group) and the third group with 0.2% LA (LA group). The diets were designed to have equivalent levels of c9t11 in the CLA and c9t11 groups. At 2 and 6 wk of feeding, the CLA group had significantly lower plasma triglyceride and total cholesterol concentrations than either the c9t11 or the LA groups. HDL-cholesterol did not differ among diet groups. The CLA group had significantly lower weight gain but greater food intake than either the c9t11 or the LA groups. There were no significant differences between the c9t11 and the LA groups in any of the variables measured. We conclude that under our experimental conditions of short-term feeding, c9t11, thought to be the active compound in CLA, does not produce the same effect as the isomer mixture.

The activity of the overt form of rat liver mitochondrial carnitine palmitoyltransferase or CPT0 (EC 2.3.1.21) towards different fatty acid substrates was studied. The following non-esterified fatty acids (NEFA) and their CoA esters in the presence of 1% bovine serum albumin (BSA) were tested: 16:0, 18:0, 18:1, 18:2, 18:3 omega 3, 20:4, 20:5 omega 3 and 22:6 omega 3. The data fit a square hyperbolic model for enzyme catalysis (p less than 0.001, non-linear regression). Asymptotic Vmax and K0.5, substrate concentration at one-half Vmax, were calculated using total concentrations of acyl-CoA, or unbound concentrations of NEFA. BSA was found to act as a true substrate reservoir for NEFA in that the dissociation of the NEFA-BSA complex was 10-330 times faster than the CPT0 reaction. Regardless of form (NEFA or CoA ester), 18:3 omega 3 gave the highest, while 22:6 omega 3 and 18:0 gave the lowest rates of acylcarnitine synthesis. Except for 18:3 omega 3 and 18:2, Vmax for NEFA was generally lower than for acyl-CoA, with the greatest differences observed for 20:4, 20:5 omega 3 and 22:6 omega 3, suggesting that acyl-CoA synthesis may also be important in the control of the entry of these fatty acids into the mitochondria. The data provide an enzymatic rationale for the relatively low content of 18:3 omega 3 in esterified lipid.

Rat adipose hormone-sensitive lipase-mediated release of fatty acids from triglycerides was studied in three model systems: i) cultured preadipocytes containing polyunsaturated fatty acid-enriched triglyceride; ii) perfused epididymal fat pads; and iii) in vitro incubations of crude preparations of hormone-sensitive lipase with synthetic triglyceride-analogues as substrates. We found that cultured preadipocytes challenged with 10 microM norepinephrine tended to release more omega 6 and omega 3 polyunsaturated fatty acids than saturated fatty acids. Fat pads perfused with 10 microM norepinephrine preferentially released arachidonate and alpha-linolenate but tended to retain oleate and linoleate. Finally, crude preparations of hormone-sensitive lipase released from the triglyceride-analogue substrates alpha-linolenate twice as fast as oleate. We conclude that rat adipose hormone-sensitive lipase preferentially releases polyunsaturated fatty acids from triglycerides. We suggest that this may be a mechanism by which these fatty acids are kept from being trapped in fat depots and maintained in the circulation.

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