title: PPARγ activation alters fatty acid composition in adipose triglyceride, in addition to proliferation of small adipocytes, in insulin resistant high-fat fed rats.
abstract: It was reported that adipocyte size is potentially correlated in part to amount of long chain polyunsaturated fatty acids (PUFAs) and insulin resistance because several long chain PUFAs can be ligands of peroxisome proliferator-activated receptors (PPARs). In our previous study, marked reduction of PUFAs was observed in insulin-resistant high-fat fed rats, which may indicate that PUFAs are consumed to improve insulin resistance. Although PPARγ agonist, well known as an insulin sensitizer, proliferates small adipocytes, the effects of PPARγ agonist on FA composition in adipose tissue have not been clarified yet. In the present study, we administered pioglitazone, a PPARγ agonist, to high-fat fed rats, and measured their FA composition of triglyceride fraction in adipose tissue and adipocyte diameters in pioglitazone-treated (PIO) and non-treated (control) rats. Insulin sensitivity was obtained with hyperinsulinemic euglycemic clamp. Average adipocyte diameter in the PIO group were smaller than that in the control one without change in tissue weight. In monounsaturated FAs (MUFAs), 14:1n-5, 16:1n-7, and 18:1n-9 contents in the PIO group were lower than those, respectively, in the control group. In contrast, 22:6n-3, 20:3n-6, 20:4n-6, and 22:4n-6 contents in the PIO group were higher than those, respectively, in the control group. Insulin sensitivity was higher in the PIO group than in the control one. These findings suggest that PPARγ activation lowered MUFAs whereas suppressed most of C20 or C22 PUFAs reduction, and that the change of fatty acid composition may be relevant with increase in small adipocytes.
authors.affiliation: Department of Biomedical Information Engineering, Graduate School of Medical Science, Yamagata University, 2-2-2, Iida-nishi, Yamagata 990-9585, Japan. Electronic address: d_sato@yz.yamagata-u.ac.jp.
authors.forename: Daisuke
authors.initials: D
authors.lastname: Sato
authors.affiliation: Department of Biomedical Information Engineering, Graduate School of Medical Science, Yamagata University, 2-2-2, Iida-nishi, Yamagata 990-9585, Japan.
authors.forename: Kanako
authors.initials: K
authors.lastname: Oda
authors.affiliation: Research Center of Health, Physical Fitness and Sports, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8601, Japan. Electronic address: info@tonyo.jp.
authors.forename: Masataka
authors.initials: M
authors.lastname: Kusunoki
authors.affiliation: Department of Materials and Applied Chemistry, College of Science and Technology, Nihon University, 1-8-14, Kandasurugadai, Chiyoda-ku, Tokyo 101-8308, Japan. Electronic address: nishina.atsuyoshi@nihon-u.ac.jp.
authors.forename: Atsuyoshi
authors.initials: A
authors.lastname: Nishina
authors.affiliation: Department of Health and Nutrition, Yamagata Prefectural Yonezawa University of Nutrition Sciences, 6-15-1, Tohrimachi, Yonezawa 992-0025, Japan. Electronic address: k-takahashi@yone.ac.jp.
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Takahashi
authors.affiliation: Department of Bio-Systems Engineering, Graduate School of Science and Engineering, Yamagata University, 4-3-16, Johnan, Yonezawa 992-8510, Japan. Electronic address: zhgfeng@yz.yamagata-u.ac.jp.
authors.forename: Zhonggang
authors.initials: Z
authors.lastname: Feng
authors.affiliation: Okinaka Memorial Institute for Medical Research, 2-2-2, Toranomon, Minato-ku, Tokyo 105-8470, Japan. Electronic address: kazu4786@chive.ocn.ne.jp.
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Tsutsumi
authors.affiliation: Department of Biomedical Information Engineering, Graduate School of Medical Science, Yamagata University, 2-2-2, Iida-nishi, Yamagata 990-9585, Japan. Electronic address: task-n@yz.yamagata-u.ac.jp.
authors.forename: Takao
authors.initials: T
authors.lastname: Nakamura
mesh_terms: D017667:Adipocytes / Q000187:drug effects* / Q000473:pathology; D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001823:Body Composition / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D048429:Cell Size / Q000187:drug effects; D059305:Diet, High-Fat / Q000009:adverse effects*; D005227:Fatty Acids / Q000737:chemistry* / Q000378:metabolism; D007333:Insulin Resistance; D008297:Male; D047495:PPAR gamma / Q000819:agonists*; D000077205:Pioglitazone; D051381:Rats; D017208:Rats, Wistar; D045162:Thiazolidinediones / Q000494:pharmacology*; D014280:Triglycerides / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; D005227:Fatty Acids; D047495:PPAR gamma; D045162:Thiazolidinediones; D014280:Triglycerides; D000077205:Pioglitazone
keywords: Adipocyte size; Fatty acid composition; Insulin resistance; Peroxisome proliferator-activated receptor γ; Thiazolidinedione