title: Dietary palatinose and oleic acid ameliorate disorders of glucose and lipid metabolism in Zucker fatty rats.
abstract: Excessive dietary intake of carbohydrates and fats has been linked to the development of obesity. However, the mechanism by which these dietary factors interact to bring about metabolic changes has not been elucidated. We examined the combined effects of different types of dietary carbohydrates and fats on the etiology of obesity and its complications in the Zucker fatty (fa/fa) rat, a model of obesity. Specifically, these rats were fed an isocaloric diet containing various combinations of carbohydrates [palatinose (P), an insulin-sparing sucrose analogue, and sucrose (S)] and fatty acids [oleic acid (O) and linoleic acid (L)]. After 8 wk, palatinose feeding (PO and PL) led to significant reductions in visceral fat mass, adipocyte cell size, hyperglycemia, and hyperlipidemia compared with sucrose feeding (SO and SL); pancreatic islet hypertrophy was also prevented by palatinose feeding. Linoleic-acid-fed rats (PL and SL) exhibited reduced insulin-immunoreactive staining of the pancreatic islets, enhanced macrophage infiltration in adipose tissue, and an elevated plasma tumor necrosis factor-alpha concentration when compared with oleic-acid-fed rats (PO and SO). Furthermore, sucrose and linoleic acid synergistically increased the expression of genes involved in hepatic gluconeogenesis and lipogenesis [sterol regulatory-element binding protein (SREBP)-1c and SREBP-2]. In conclusion, a diet containing palatinose and oleic acid may prevent diet-induced metabolic abnormalities. The combination of palatinose and oleic acid holds promise for a new approach to preventing and treating obesity and its complications.
authors.affiliation: Department of Clinical Nutrition, Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima 770-8503, Japan.
authors.forename: Kazusa
authors.initials: K
authors.lastname: Sato
authors.forename: Hidekazu
authors.initials: H
authors.lastname: Arai
authors.forename: Akira
authors.initials: A
authors.lastname: Mizuno
authors.forename: Makiko
authors.initials: M
authors.lastname: Fukaya
authors.forename: Tadatoshi
authors.initials: T
authors.lastname: Sato
authors.forename: Megumi
authors.initials: M
authors.lastname: Koganei
authors.forename: Hajime
authors.initials: H
authors.lastname: Sasaki
authors.forename: Hironori
authors.initials: H
authors.lastname: Yamamoto
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Taketani
authors.forename: Toshio
authors.initials: T
authors.lastname: Doi
authors.forename: Eiji
authors.initials: E
authors.lastname: Takeda
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects / Q000473:pathology; D000818:Animals; D001786:Blood Glucose / Q000187:drug effects; D001835:Body Weight; D004032:Diet; D005786:Gene Expression Regulation / Q000187:drug effects; D005947:Glucose / Q000378:metabolism*; D007249:Inflammation / Q000473:pathology; D007534:Isomaltose / Q000031:analogs & derivatives* / Q000494:pharmacology; D050356:Lipid Metabolism / Q000187:drug effects*; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D019301:Oleic Acid / Q000494:pharmacology*; D010179:Pancreas / Q000187:drug effects; D051381:Rats; D011924:Rats, Zucker; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D014280:Triglycerides; D019301:Oleic Acid; D007534:Isomaltose; D005947:Glucose; C008189:isomaltulose