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Insulin resistance improving agents

外国特許コード F110003334
整理番号 A192-07US2
掲載日 2011年6月22日
出願国 アメリカ合衆国
出願番号 04127908
公報番号 20100120674
公報番号 7850976
出願日 平成20年3月3日(2008.3.3)
公報発行日 平成22年5月13日(2010.5.13)
公報発行日 平成22年12月14日(2010.12.14)
国際出願番号 JP2002007599
国際公開番号 WO2003063894
国際出願日 平成14年7月26日(2002.7.26)
国際公開日 平成15年8月7日(2003.8.7)
優先権データ
  • 特願2002-023554 (2002.1.31) JP
  • 10/502,051 (2004.7.30) US
  • 2002JP007599 (2002.7.26) WO
発明の名称 (英語) Insulin resistance improving agents
発明の概要(英語) 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).
従来技術、競合技術の概要(英語) BACKGROUND ART
Hitherto, adipose tissue has been considered a mere storage medium for excess energy.
However, recent research has elucidated that adipose tissue produces and secretes a variety of physiologically active substances.
The physiologically active substances are collectively called adipocytokines, and specific members which have been known to date include leptin, tumor necrosis factor-alpha (TNF-alpha ), plasminogen-activator inhibitor type 1 (PAI-1), adipsin, and resistin.
Some of these adipocytokines, such as leptin, TNF-alpha , and resistin, have been suggested to be secreted from adipocytes to thereby control sensitivity to insulin.
Adiponectin has recently been identified as an adipocytokine.
Adiponectin was originally identified independently by four research groups that used different approaches.
Adiponectin cDNA was isolated by large-scale random sequencing of a 3'-directed, human-adipose-tissue cDNA library.
Mouse cDNAs for adiponectin termed AcrpSO and AdipoQ were cloned through differential display before and after differentiation of mouse 3T3-L1 and 3T3-F442A cells, respectively.
Human adiponectin was also purified from plasma as gelatin-binding protein 28.
Obese/diabetic mice and humans exhibit significantly reduced levels of mRNA expression of adiponectin and plasma adiponectin.
Lodish et al. have recently reported that a proteolytic cleavage product of Acrp30 increases fatty-acid oxidation in muscle and causes weight loss in mice.
However, whether or not adiponectin is effective in the actual treatment of diabetes remains unknown.
Insulin resistance induced by high-fat diet and accompanied with obesity is a major risk factor for diabetes and cardiovascular diseases, and therefore, capacity to improve insulin resistance is a key factor for determining that a certain drug is effective for the treatment of diabetes.
Accordingly, an object of the present invention is to provide a novel drug which improves insulin resistance and thus is useful in the treatment of diabetes.

特許請求の範囲(英語) [claim1]
1. A method for treating insulin resistance in a subject in need thereof comprising administering an effective amount of an agent containing, as an active component, a C-terminal globular domain of adiponectin consisting of amino acid residues 111 to 242 of SEQ ID NO: 2 or 114 to 239 of SEQ ID NO: 2.
[claim2]
2. The method of claim 1, wherein said agent further comprises a pharmacologically acceptable carrier.
[claim3]
3. The method of claim 2, wherein said pharmacologically acceptable carrier is selected from the group consisting of distilled water, a solubilizer, a stabilizer, an emulsifier, and a buffer.
[claim4]
4. The method of claim 1, wherein said administering is by injection.
[claim5]
5. The method of claim 1, wherein said effective amount ranges from 0.1 mu g/day to 10 mg/day based on the amount of adiponectin.
[claim6]
6. The method of claim 1, wherein said C-terminal globular domain of adiponectin consists of amino acid residues 111 to 242 of SEQ ID NO: 2.
[claim7]
7. The method of claim 1, wherein said C-terminal globular domain of adiponectin consists of amino acid residues 114 to 239 of SEQ ID NO: 2.
[claim8]
8. A method for treating type 2 diabetes in a subject in need thereof comprising administering an effective amount of a therapeutic agent for type 2 diabetes containing, as an active component, a C-terminal globular domain of adiponectin consisting of amino acid residues 111 to 242 of SEQ ID NO: 2 or 114 to 239 of SEQ ID NO: 2.
[claim9]
9. The method of claim 8, wherein said agent further comprises a pharmacologically acceptable carrier.
[claim10]
10. The method of claim 9, wherein said pharmacologically acceptable carrier is selected from the group consisting of distilled water, a solubilizer, a stabilizer, an emulsifier, and a buffer.
[claim11]
11. The method of claim 8, wherein said administering is by injection.
[claim12]
12. The method of claim 8, wherein said effective amount ranges from 0.1 mu g/day to 10 mg/day.
[claim13]
13. The method of claim 8, wherein said C-terminal globular domain of adiponectin consists of amino acid residues 111 to 242 of SEQ ID NO: 2.
[claim14]
14. The method of claim 8, wherein said C-terminal globular domain of adiponectin consists of amino acid residues 114 to 239 of SEQ ID NO: 2.
  • 発明者/出願人(英語)
  • KADOWAKI TAKASHI
  • YAMAUCHI TOSHIMASA
  • KAMON JUNJI
  • WAKI HIRONORI
  • NAGAI RYOZO
  • KIMURA SATOSHI
  • TOMITA MOTOO
  • JAPAN SCIENCE AND TECHNOLOGY AGENCY
国際特許分類(IPC)
米国特許分類/主・副
  • 424/198.1
  • 514/6.7
  • 530/399
参考情報 (研究プロジェクト等) CREST Development, Differentiation, and Regeneration in Biological Systems AREA
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