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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.

This review focuses on the possible association between types of fatty acids and weight change. It examines the biological plausibility underlining these associations and the evidence obtained to date from clinical trials and epidemiological studies. Animal studies have shown that dietary short-and medium-chain fatty acids compared to long-chain fatty acids appear to promote weight loss. Similarly, monounsaturated fatty acids (MUFAs) appear to favor weight loss compared to saturated fatty acids (SFAs) in human studies. The structure of fatty acids seems to affect their degree of oxidation and deposition. Although results are conflicting, human studies follow the general trend reported in animal studies. These trials suggest that some fatty acids are prone to oxidation and some others lead to fat storage when comparing isocaloric diets. For instance, n-3 polyunsaturated fatty acids (PUFAs), eicosapentaenoic and docosahexaenoic acids are preferentially oxidizied to other PUFA but results remain inconsistent. Epidemiological studies concerning this issue reported that total dietary fat, which includes MUFA, PUFA, and SFA could increase the risk of obesity, but results are few and conflicting. The rising biological plausibility linking dietary fat quality and risk of obesity, together with the rather recent addition of fatty acids content in food composition tables, support the need for major epidemiological studies in that area.Obesity (2008) 16, 7-15.

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.

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