title: Dietary palmitic acid influences LDL-mediated lymphocyte proliferation differently to other mono- and polyunsaturated fatty acids in rats.
abstract: Recent studies suggest that the biological effects of saturated fatty acids depend on the length of their chain. We compared the effect of diets containing different fatty acids on plasma lipids and lymphocyte proliferation in the presence of lovastatin and with increasing amounts of LDL. Lymphocytes from rats fed with a diet rich in palmitic acid had a greater lymphocyte proliferation capacity than those from rats fed with diets rich in oleic acid, linoleic acid, or fish oil. This effect was maintained when small amounts of polyunsaturatwed fatty acids (PUFA; sunflower oil) were added to the palmitic acid diet. LDL receptor activity, measured by the capacity of lovastatin to revert the inhibition of lymphocyte proliferation with increasing amounts of LDL in the medium, was greater in the rats fed with palmitic acid, and was similar to the other groups when small amounts of PUFA were added. All the groups had similar levels of plasma cholesterol, but the LDL levels were significantly lower in the group fed with palmitic acid plus PUFA. The highest HDL-cholesterol (HDLc) levels were found in the palmitic acid group and the lowest LDL-cholesterol (LDLc)/HDLc ratio in the palmitic acid plus PUFA group. These results suggest that diets rich in palmitic acid do not raise total cholesterol, but reduce LDLc or keep it normal, and raise HDLc levels. This effect may be partly due to an increase in LDL receptor activity. The inclusion of small amounts of PUFA in the diet rich in palmitic acid substantially modified the LDL receptor response in the lymphocytes, suggesting that the proportion of different families of dietary fatty acids may be more important than the individual amount of each in absolute terms to explain their effects on plasma lipids and lipoproteins.
authors.affiliation: Endocrinology and Nutrition Service, Carlos Haya Hospital Complex, Malaga, Spain.
authors.forename: F J
authors.initials: FJ
authors.lastname: Tinahones
authors.forename: J M
authors.initials: JM
authors.lastname: Gómez-Zumaquero
authors.forename: A
authors.initials: A
authors.lastname: Monzón
authors.forename: G
authors.initials: G
authors.lastname: Rojo-Martínez
authors.forename: A
authors.initials: A
authors.lastname: Pareja
authors.forename: S
authors.initials: S
authors.lastname: Morcillo
authors.forename: F
authors.initials: F
authors.lastname: Cardona
authors.forename: G
authors.initials: G
authors.lastname: Olveira
authors.forename: F
authors.initials: F
authors.lastname: Soriguer
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000924:Anticholesteremic Agents / Q000494:pharmacology; D049109:Cell Proliferation / Q000187:drug effects; D004041:Dietary Fats / Q000008:administration & dosage* / Q000494:pharmacology; D005229:Fatty Acids, Monounsaturated / Q000008:administration & dosage / Q000494:pharmacology; D005231:Fatty Acids, Unsaturated / Q000008:administration & dosage / Q000494:pharmacology; D008055:Lipids / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood / Q000502:physiology*; D008148:Lovastatin / Q000494:pharmacology; D008214:Lymphocytes / Q000737:chemistry / Q000166:cytology / Q000187:drug effects*; D008297:Male; D019308:Palmitic Acid / Q000008:administration & dosage* / Q000494:pharmacology; D010743:Phospholipids / Q000737:chemistry; D051381:Rats; D017208:Rats, Wistar; D011973:Receptors, LDL / Q000378:metabolism*; D013936:Thymidine / Q000378:metabolism; D013950:Thymus Gland / Q000166:cytology; D014316:Tritium
chemical_list: D000924:Anticholesteremic Agents; D004041:Dietary Fats; D005229:Fatty Acids, Monounsaturated; D005231:Fatty Acids, Unsaturated; D008055:Lipids; D008077:Lipoproteins, LDL; D010743:Phospholipids; D011973:Receptors, LDL; D014316:Tritium; D019308:Palmitic Acid; D008148:Lovastatin; D013936:Thymidine