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Dual-therapy strategy for modification of adiponectin receptor signaling in aging-associated chronic diseases

Masaaki Waragai1, Gilbert Ho2, Yoshiki Takamatsu1

  • 1Tokyo Metropolitan Institute of Medical Science, 2-1-6 Kamikitazawa, Setagaya-ku, Tokyo, Japan.

Drug Discovery Today
|May 11, 2018
PubMed

Insights

Adiponectin (APN) is key in metabolic syndrome but elevated in Alzheimer's, heart, and kidney diseases. APN receptor antagonists may treat these conditions, unlike metabolic syndrome therapies.

Area of Science:

  • Endocrinology
  • Metabolic Disorders
  • Neurodegenerative Diseases

Background:

  • Adiponectin (APN) is an adipocyte-derived hormone that sensitizes insulin receptor signaling.
  • Metabolic syndrome is associated with low APN levels, while Alzheimer's disease (AD), chronic heart failure (CHF), and chronic kidney disease (CKD) show hyperadiponectinemia.
  • The APN/obesity paradox suggests reduced APN may benefit these chronic diseases.

Purpose of the Study:

  • To explore the distinct roles of adiponectin in metabolic syndrome versus other chronic diseases.
  • To investigate the potential therapeutic benefit of targeting adiponectin in AD, CHF, and CKD.

Main Methods:

  • Review of existing literature on adiponectin levels and therapeutic targets in metabolic syndrome, AD, CHF, and CKD.
  • Comparative analysis of adiponectin's role in insulin resistance versus its paradoxical association with other chronic conditions.

Main Results:

  • Adiponectin (APN) levels are inversely correlated with insulin resistance in metabolic syndrome.
  • Hyperadiponectinemia is observed in Alzheimer's disease, chronic heart failure, and chronic kidney disease.
  • The APN/obesity paradox is noted in these chronic diseases, suggesting a different therapeutic approach.

Conclusions:

  • Therapeutic strategies for metabolic syndrome targeting adiponectin may differ from those for AD, CHF, and CKD.
  • Adiponectin receptor antagonists are proposed as a potential therapeutic strategy for chronic diseases characterized by hyperadiponectinemia.

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