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Updated: Oct 8, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
08:34

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Paradoxical decrease of an adipose-specific protein, adiponectin, in obesity

Y Arita1, S Kihara, N Ouchi

  • 1Graduate School of Medicine, Institute for Molecular and Cellular Biology, Osaka University, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.

Biochemical and Biophysical Research Communications
|March 27, 1999
PubMed

Insights

Researchers identified adiponectin, a key protein from fat cells. Lower adiponectin levels were found in obese individuals, suggesting its role in metabolic health.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Endocrinology

Background:

  • The apM1 gene is the most abundant adipose-specific transcript in humans.
  • Its gene product, adiponectin, is a soluble matrix protein.
  • Adiponectin plays a crucial role in metabolic regulation.

Purpose of the Study:

  • To develop a method for quantifying plasma adiponectin concentration.
  • To investigate the physiological and pathophysiological roles of adiponectin in humans.

Main Methods:

  • Production of monoclonal and polyclonal antibodies for human adiponectin.
  • Development of an enzyme-linked immunosorbent assay (ELISA) system for adiponectin quantification.

Main Results:

  • Adiponectin is abundantly present in the plasma of healthy volunteers (1.9–17.0 mg/ml).
  • Plasma adiponectin concentrations are significantly lower in obese subjects compared to non-obese subjects.
  • Adiponectin is exclusively secreted from adipose tissue.

Conclusions:

  • The developed ELISA system is a valuable tool for measuring adiponectin levels.
  • This assay will aid in understanding the physiological and pathophysiological significance of adiponectin in human health and disease.
  • Reduced adiponectin may be linked to obesity and associated metabolic dysfunctions.

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