Toudai Tlo, Ltd.

Nissan Chemical Industries Limited

Japan Science and Technology Agency

The University of Tokyo

Sekisui Medical Co., Ltd.

Daiichi Pure Chemicals Co., Ltd.

Toray Industries, Inc.

Riken Corporation

Takashi Kadowaki

Shigeyuki Yokoyama

Toshimasa Yamauchi

Ryozo Nagai

Junji Kamon

Osamu Miyazaki

Hiroyuki Ebinuma

Hirokazu Yago

Yuka Akimoto

Kazuo Hara

Tetsuya Kubota

Naoto Kubota

Takehiro Takahashi

Satoshi Kimura

Yasushi Imai

Tetsuo Noda

Hiroki Kumagai

Teruki Honma

Hironori Waki

Kohjiro Ueki

Motoo Tomita

Shoko Kitajima

Yukiko Okazaki

Yusuke Ito

Matthias Bluher

Yasuo Terauchi

Sumiko Ozawa

Jyunji Nissan Chemical Industries Ltd Kamon

Masato Iwabu

Miki Iwabu

Jyunji Kamon

Osamu Myazaki

A therapeutic or prophylactic agent for diabetes includes a thiazolidine derivative as a PPAR-&#x3b3; agonist as an effective component which exhibits a reduced side effect of the PPAR-&#x3b3; agonist. The therapeutic or prophylactic agent for diabetes includes a particular IP agonist such as beraprost sodium (BPS), and a thiazolidine derivative such as pioglitazone or a pharmaceutically acceptable salt thereof. Since the therapeutic or prophylactic agent exhibits a sufficiently effective hypoglycemic action without being accompanied by side effects characteristic to PPAR-&#x3b3; agonists, the agent is useful as a highly safe and effective therapeutic or prophylactic agent for diabetes.

Therapeutic or prophylactic agent for diabetes

Provided are a means for the prevention and treatment of obesity and/or insulin resistance and, particularly, pharmaceutical drugs for the treatment of obesity and/or insulin resistance under the influence of Follistatin-like 3 (FSTL3). Specifically, provided is an insulin resistance improving drug comprising an FSTL3 inhibitor as an active ingredient, particularly, the insulin resistance improving drug, wherein the FSTL3 inhibitor is one of (A) a substance specifically binding to FSTL3 to inhibit or suppress a function of FSTL3, (B) an inhibitor for expression of FSTL3, and (C) a competitor of FSTL3.

Insulin-resistance-improving drug

The object is to isolate and identify human and mouse adiponectin receptors, to provide a novel protein having adiponectin binding ability, and to provide a screening method and screening kit for a ligand, agonist and antagonist to an adiponectin receptor using such protein. To achieve this object, a protein is used, as novel protein having adiponectin binding ability, that is (a) a protein comprising an amino acid sequence according to Seq. No. 2, 4, 6 or 8, or (b) a protein comprising an amino acid sequence according to Seq. No. 2, 4, 6 or 8 with one or more amino acids deleted, replaced or added, and having adiponectin binding ability.

Adiponectin receptor and gene encoding the same

Kits and methods for selectively assaying a target adiponectin multimer in a biological sample. Such methods accurately evaluate the relationship between a disease and adiponectin through selective assay of adiponectin multimers and provide information that cannot be obtained through measurement of the total amount of adiponectin alone. A method for selectively assaying a target adiponectin multimer in a biological sample comprising distinguishing target adiponectin multimer from the other adiponectin multimers by using a protease and/or an antibody.

Method of selectively assaying adiponectin multimers

The invention provides an insulin resistance improving agent and a therapeutic agent for type 2 diabetes, which contain a C-terminal globular domain of adiponectin, adiponectin, or a gene for the domain or adiponectin. The invention also provides a method for improving insulin resistance and treating type 2 diabetes by administering the aforementioned agent(s).

Insulin resistance improving agents

The invention provides a method of pretreating a sample for conveniently, quickly and accurately measuring the total amount of adiponectin present in a biological sample contaminated with various adiponectin multimers. The method of measuring an sample for immunologically assaying the total amount of adiponectin present in the sample comprises reacting, with an adiponectin-containing sample, at least one of a reducing agent, an acid or a salt thereof, a surfactant, and a protease.

Mehod of pretreating sample and immunological assay method using the same

The present invention provides adiponectin expression-inducing agents, and therapeutic agents using the same for obesity and obesity-related diseases such as cardiovascular diseases or metabolic diseases, as well as methods of searching for adiponectin expression-inducing agents. KLF9, which can bind to the 32-bp fragment of position &#x2212;188 to position &#x2212;157 from the adiponectin expression start site, was demonstrated to enhance adiponectin promoter activity. Therefore, the present invention uses KLF9 as an adiponectin expression-inducing agent, and suggests that KLF9 replenishment therapy is useful for preventing and/or treating obesity or obesity-related diseases including metabolic diseases such as insulin resistance and type II diabetes, and cardiovascular diseases.

Adiponectin expression-inducing agents and uses thereof

Methods for selectively assaying a target adiponectin multimer in a biological sample. Such methods accurately evaluate the relationship between a disease and adiponectin through selective assay of adiponectin multimers and provide information that cannot be obtained through measurement of the total amount of adiponectin alone. A method for selectively assaying of a target adiponectin multimer in a biological sample comprising distinguishing target adiponectin multimer from the other adiponectin multimers by using a protease and/or an antibody.

A scavenger receptor A expression down-regulator and a drug for preventing or treating arteriosclerosis which contain, as the active ingredient, a C-terminal globular domain of adiponectin, adiponectin, or a gene encoding the domain or adiponectin. According to the present invention, there is provided a preventive or therapeutic agent capable of directly preventing intimal thickening, which constitutes an essential feature of arteriosclerosis. This effect can be attained through arresting the onset and development of arteriosclerosis by reducing the expression level of scavenger receptor A in arterial walls and preventing lipid buildup in macrophages.

Method for treating arteriosclerosis

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Tokyo, Japan

Takashi Kadowaki