Postprandial effects of a lipid-rich meal in the rat are modulated by the degree of unsaturation of 18C fatty acids.
The fatty acid composition of high-fat diets is known to influence the magnitude of postprandial events that increase the risk of metabolic syndrome. These variations in magnitude may be directly ascribed to differences in the channeling of lipids toward oxidation or storage. A study was designed to compare the effects of 4 dietary fats on postprandial energy expenditure and on some risk factors of the metabolic syndrome. To avoid usual confounding factors due to simultaneous variations in chain length and double-bounds number of fatty acids, dietary fats were chosen to provide mainly 18-carbon fatty acids with 0 (stearic acid [SA]), 1 (oleic acid [OA]), 2 (linoleic acid [LA]), or 3 (alpha-linolenic acid [ALA]) double bounds. They were given as single high-fat test meals to 4 different groups of male rats. The resting metabolic rate and the lipid and carbohydrate oxidation were measured from oxygen consumption and carbon dioxide production using indirect calorimetry 2 hours before and 6.5 hours after the test meal. Plasma glucose, triglyceride, and chylomicron concentrations were determined at 0, 1.5, and 4 hours after the test meal. Postprandial concentration of glucose and triglyceride did not vary with the nature of the test meals, whereas that of chylomicrons was the highest after the LA test meal and the lowest after the SA test meal. Postprandial increase in resting metabolic rate was the highest after the LA and OA test meals, and the lowest after the SA and ALA test meals. Compared with the 3 other diets, the ALA test meal enhanced lipid oxidation and decreased glucose oxidation during the early postprandial period (0.25-3.25 hours). This suggests that stearic acid may not induce all the adverse effects classically described for other saturated fatty acids and that alpha-linolenic acid may beneficially influence energy partitioning, especially during the early postprandial state.
Even
Patrick
P
INRA, UMR914 Nutrition Physiology and Ingestive Behavior, F-75005 Paris, France.
Mariotti
François
F
Hermier
Dominique
D
D000818:Animals; D001481:Basal Metabolism / Q000187:drug effects; D001786:Blood Glucose / Q000032:analysis; D002153:Calorimetry, Indirect; D002245:Carbon Dioxide / Q000032:analysis; D004041:Dietary Fats / Q000008:administration & dosage*; D004734:Energy Metabolism / Q000187:drug effects*; D005231:Fatty Acids, Unsaturated / Q000008:administration & dosage* / Q000737:chemistry*; D019787:Linoleic Acid / Q000008:administration & dosage; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D024821:Metabolic Syndrome / Q000209:etiology; D019301:Oleic Acid / Q000008:administration & dosage; D010101:Oxygen Consumption; D051381:Rats; D017208:Rats, Wistar; D012307:Risk Factors; D013229:Stearic Acids / Q000008:administration & dosage; D014280:Triglycerides / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D017962:alpha-Linolenic Acid / Q000008:administration & dosage
D001786:Blood Glucose; D004041:Dietary Fats; D005231:Fatty Acids, Unsaturated; D013229:Stearic Acids; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D017962:alpha-Linolenic Acid; D002245:Carbon Dioxide; D019301:Oleic Acid; C031183:stearic acid; D019787:Linoleic Acid