Six healthy adult males were fed four different diets to determine the effects of the quantity of fat (30% or 40% of energy as fat) and type of fat (polyunsaturated or saturated) on utilization of fatty acids. Each diet was fed for 15 d. The ratio of dietary polyunsaturated to saturated fat (P:S) was formulated at either 0.2 or 1.0 at both fat intakes. Subjects provided breath tests to measure background 13C and response to [1-13C]10:0 and [1-13C]16:0 fed with a test meal. Increasing the P:S increased whole-body oxidation of labeled 10:0 by 30% after consumption of both low- and high-fat diets. When labeled 16:0 was fed, the amount of 13C excreted in breath increased by a factor of 2.4 after the low-fat diet with a high P:S compared with the diet with a low P:S. The results suggest that the amount and type of fat in the diet affect utilization of individual fatty acids in normal subjects.

The objective of this study was to quantitatively measure the essential fatty acid pools in lipid fractions of plasma lipoproteins and the alteration of these pool sizes after consumption of a physiologic intake of fish oil. Twenty-three cystic fibrosis (CF) patients and 21 normal subjects were supplemented with fish oil, providing 35 mg n-3 fatty acids/kg body wt for 4 wk. Blood was collected pre- and postsupplementation and was quantitatively analyzed to determine the fatty acid pool size in each lipid class of low-density lipoproteins (LDLs), high-density lipoproteins (HDLs), and very-low-density lipoproteins. Two 7-d food records were collected to determine total fat and fatty acid intakes. Intakes of protein, carbohydrate, and fat as a percentage of energy and the ratio of polyunsaturated to saturated fats was similar for the CF and control groups. Energy intake was greater for CF subjects. Smaller lipoprotein essential fatty acid pools were observed in CF patients than in control subjects. Healthy subjects had larger essential fatty acid pool sizes in cholesterol ester fractions of HDLs and LDLs than CF subjects. Cholesterol ester and phosphatidylcholine pools transported the majority of essential fatty acids in both CF and control subjects.

To investigate the effect of increasing dietary polyunsaturated fat intake on fat absorption in Crohn's patients, normal subjects and subjects with inactive Crohn's disease consumed a high polyunsaturated to saturated fat ratio diet. Subjects participated in breath tests before and after six months of a high polyunsaturated to saturated (P/S) fat ratio diet to measure their response to [1-13C] 10:0 and [1-13C] 16:0 ingested with a test meal. Whole body absorption-oxidation of C10:0 was not affected by the diet treatment. Before diet treatment, whole body absorption-oxidation of C16:0 in Crohn's patients was 80% of that observed for control subjects. After consuming a high polyunsaturated to saturated fatty acid ratio diet, subjects increased oxidation of C16:0 by 85% compared to before the diet treatment period. It is concluded that (1) absorption of labelled C16:0 from a test meal is reduced in Crohn's patients, and (2) consumption of a high polyunsaturated to saturated fatty acid ratio diet improves the utilization of dietary C16:0 by Crohn's patients.

Chain shortening of palmitic acid was examined in vivo by comparing oxidation rates of [1-13C]palmitate vs [16-13C]palmitate fed to four male subjects consuming a high-fat diet. For 9 d subjects were fed a diet of normal foods providing an energy intake equal to their estimated requirements. The diet provided (as energy) approximately 14% protein, 46% carbohydrate, and 40% fat at a P:S ratio of 0.25. Analysis of breath 13CO2 enrichment on day 3 permitted analysis of background 13C contribution from the test diet alone. On days 4 and 7 either [1-13C]palmitic acid or [16-13C]palmitic acid (9-13.5 mg/kg body wt) was fed with the breakfast meal. The whole-body rate of oxidation of [1-13C]palmitic acid was significantly greater than that observed for [16-13C]palmitic acid. These results suggest that up to 34% of dietary palmitic acid consumed may be subjected to extramitochondrial chain shortening.