It is a widely accepted model of nutrient balance that the metabolic handling of fat energy is likely to induce a positive energy balance mainly because of the inability of dietary fat to promote fat oxidation [16, 17]. Indeed several studies suggest that dietary fat intake and genotype interact to regulate fat deposition [18, 19]. It is an open question, however, whether it is possible to affect the fatty acid profile in the blood plasma by stimulating the fatty acid oxidation with an experimental high fat formula containing MCFA in combination with n-3 LCPUFA but without LCFA. Due to its unique absorption and metabolic characteristics, MCFA oil, consisting of saturated fatty acids with 8–12 carbons, has been used therapeutically since the 1950s in the treatment of fat malabsorption, cystic fibrosis, epilepsy, weight control and to increase exercise performance. Dietary n-3 LCPUFA on the other side have been identified to influence the serum and red blood cell membrane fatty acid composition  and to stimulate the peroxisomal β-oxidation  resulting in an increased basal lipid oxidation.
Furthermore, it has been shown that n-3 LCPUFA are an environmental factor in the regulation of body mass reduction . Especially, eicosapentaenoic acid has been suggested to induce the peroxisome proliferator-activated receptor gamma-1 as a key regulator of adipocytes differentiation, lipid metabolism and insulin resistance . Thus, both MCFA and dietary lipids containing n-3 LCPUFA are candidates to stimulate the hepatocellular β-oxidation. The results of the present short term intervention study indicate that a combination of MCFA and n-3 LCPUFA but missing LCFA effected a significant reduction of total plasma triacylglycerols probably due to an increased β;-oxidation of fatty acids. The extent of this reduction was higher than it could be suspected from the individual MCFA or LCPUFA implications on lipid oxidation alone suggesting synergetic effects. Previous Studies in animals  and with infants  suggested that dietary n-3 LCPUFA could decrease the hepatic excretion of cholesterol and biliary cholesterol nucleation time in obese women .
In the present trial the cholesterol concentration decreased in both groups due to the cholesterol free diet with no significant differences between the groups.
The study also showed a specific effect of the test formula on the plasma fatty acid pattern in comparison to the control. Dietary n-6 and n-3 fatty acids have opposing physiological functions concerning homeostasis, normal development of organs and tissues, inflammation and mental health . On condition that the normal western diet is unbalanced in the n-3 to n-6 fatty acid ratio, it might be necessary to decrease the intake of n-6 fatty acids and increase the n-3 fatty acid intake. Tissue arachidonic acid pools originate from the diet and from the hepatic and extrahepatic desaturation-elongation of dietary linoleic acid. Particularly during fasting linoleic acid is an important substrate (27). To affect the n-3 to n-6 ratio shift the experimental fat blend contains sufficient amounts of α-linolenic acid which daily requirement is 1.5 g C18:3 n-3/day [27, 28], but less linoleic acid compared to the placebo (Table 2). Arachidonic acid increased in the test group and the essential linoleic acid concurrenly decreased, eicosapentaenoic acid and docosahexaenoic acid (C 22:6 n-3) increased (not shown) implying a significant increase of the n-3 to n-6 LCPUFA ratio in the test group compared to the control. This dietary influence on the plasma fatty acid profile was already pronounced at day 4, although the maximum effect was observed at day 15.
Several studies with comparable fish oil supplementations indicated significant eicosapentaenoic acid and docosahexaenoic acid demonstrated without extensive alterations of total plasma fatty acid profile e.g. linoleic acid was not affected [29, 30]. In our study however, the essential linoleic acid decreased in the test group suggesting that MCFA and LCPUFA without LCFA provokes a rapid blood clearance and pronounced increase of n-3/n-6 ratio.
The necessary requirement for linoleic acid is 10 g/day [27, 28]. In fact, the reduction of the linoleic acid provoked by the test fat blend is irrelevant during a short term treatment because of physiologic reserves in the fat tissue but may be questionable for long term usage. The metabolic outcome during a long term treatment have to be shown in further investigations.
To maintain human health and to support weight control efforts a variety of dietary concepts are discussed that differ exceptionally in the macronutrient content and infringe nutritional guidelines. As the administration of a high fat diet with MCFA may imply the risk of liver injury or an unbalanced glucose-protein metabolism . On this matter several physiological safety parameters were evaluated. Neither significant physiological effects on parameters for liver and kidney disorders (liver enzymes activities in the plasma and creatinine concentration in the urine) nor indicators of muscle decomposition (urea concentration in the urine) or pancreas injury values (lipase-activity in the plasma) could be detected. In contrast to observations that LCPUFA could increase the basal glucose level of plasma , the plasma glucose-level of both test groups decreased within the physiological range. In summary, these data indicate that the experimental formula is safe concerning glucose metabolism, protein digestion, liver and kidney function.
With respect to acceptance of hypoenergetic diets the subjective feeling of satiety is always relevant. Carbohydrates may play a greater role for the duration of satiety than does fat but several studies suggested that MCFA are important for other aspects of the control of food intake, especially in satiation at the next meal . In this short term intervention all volunteers reported about their satiety with both formulas possibly due to the high fat content of the trial products.
Adult obesity is a health hazard because of its association with numerous metabolic complications , but also childhood obesity is the basis of coronary heart disease risk and mortality in adulthood . From studies in post-obese individuals it is well known that these individuals normally have low rates of fat oxidation that may explain their risk to regain weight . Additionally, it has been postulated that weight loss distinct from energy restriction is associated with improvements in serum lipid levels. In this present study the fat mass reduced significantly in the test group but also in the control group. In contrast to the altered n-3 to n-6 LCPUFA ratio in plasma in the test group, the concentration of storage fatty acids like palmitic acid (C 16:0) (not shown) and stearic acid remained in the homeostasis despite missing LCFA in the test formula indicated a LCFA release from adipocytes.
Therefore, the rapid clearance of blood fat induced by an increased stimulation of hepatocytic β-oxidation may represent a new mechanism to loose fat mass and may offer new strategies to prevent the metabolic syndrome. However, implications of the experimental fat blend against obesity have to be investigated in future studies.