title: Noninvolvement of hypertriglyceridemia and hyperleptinemia in blood pressure increases induced by dietary lard in rats.
abstract: We investigated whether hypertriglyceridemia and hyperleptinemia are involved in the development of increases in blood pressure induced by dietary lard. Rats received either chow alone or chow in which 50% of the energy content was from substituted lard. Each group was divided into two groups according to whether the diet included bezafibrate or not. In another series of experiments, rats were fed either chow alone or chow in which 50% of the energy content was from substituted lard, safflower oil, or sucrose. Systolic blood pressure (SBP) was measured every week during each 7-week feeding period. A steady-state plasma glucose method was used to determine insulin sensitivity after lard substitution with or without bezafibrate. After the 7-week feeding period, the plasma levels of glucose, immunoreactive insulin, triglyceride and leptin were measured. In rats fed with a high lard diet, SBP, plasma levels of immunoreactive insulin, triglyceride, leptin and steady-state plasma glucose concentrations significantly increased, compared with levels of these substances in controls. Bezafibrate treatment completely reversed these effects. In rats fed with a high safflower oil or a high sucrose diet, no significant change was seen in SBP and plasma immunoreactive insulin levels. However, the plasma triglyceride levels were increased by dietary lard or sucrose. Moreover, the plasma leptin level was also increased by dietary lard and safflower oil. Neither dietary hypertriglyceridemia nor hyperleptinemia were involved in the development of increases in blood pressure induced by dietary lard.
authors.affiliation: Department of Geriatrics, Medicine in Growth and Aging, Health and Community Medicine Program, Nagoya University Graduate School of Medicine, 65 Tsuruma-cho, Showa-ku, Nagoya 466-8550, Japan. ntamaya@med.nagoya-u.ac.jp
authors.forename: N
authors.initials: N
authors.lastname: Tamaya
authors.forename: K
authors.initials: K
authors.lastname: Uemura
authors.forename: S
authors.initials: S
authors.lastname: Yoshioka
authors.forename: M
authors.initials: M
authors.lastname: Ueda
authors.forename: A
authors.initials: A
authors.lastname: Hattori
authors.forename: M
authors.initials: M
authors.lastname: Kuzuya
authors.forename: Y
authors.initials: Y
authors.lastname: Ohmoto
authors.forename: M
authors.initials: M
authors.lastname: Muraguchi
authors.forename: J
authors.initials: J
authors.lastname: Nakamura
authors.forename: A
authors.initials: A
authors.lastname: Iguchi
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects; D000818:Animals; D001629:Bezafibrate / Q000494:pharmacology; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects*; D002784:Cholesterol / Q000097:blood; D004032:Diet; D004041:Dietary Fats / Q000494:pharmacology*; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology; D015228:Hypertriglyceridemia / Q000097:blood* / Q000503:physiopathology; D000960:Hypolipidemic Agents / Q000494:pharmacology; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D012450:Safflower Oil / Q000494:pharmacology
chemical_list: D001786:Blood Glucose; D004041:Dietary Fats; D000960:Hypolipidemic Agents; D007328:Insulin; D020738:Leptin; D012450:Safflower Oil; D002784:Cholesterol; D001629:Bezafibrate