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Perlecan, a heparan sulfate proteoglycan, regulates systemic metabolism with dynamic changes in adipose tissue and

Yuri Yamashita1,2, Satoshi Nakada3, Toshinori Yoshihara4

  • 1Aging Biology in Health and Disease, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan.

Scientific Reports
|May 19, 2018
PubMed

Insights

Perlecan deficiency in mice reduced white adipose tissue and prevented fatty liver, improving metabolic health. This suggests perlecan downregulation may combat obesity and metabolic syndrome.

Area of Science:

  • Biochemistry
  • Physiology
  • Molecular Biology

Background:

  • Perlecan (HSPG2) is a basement membrane heparan sulfate proteoglycan involved in various biological functions.
  • Its specific roles in obesity and metabolic syndrome are not fully understood.

Purpose of the Study:

  • To investigate the physiological roles of perlecan in obesity and metabolic syndrome.
  • To elucidate the molecular mechanisms underlying perlecan's influence on metabolic regulation.

Main Methods:

  • Utilized perinatal lethality-rescued perlecan knockout (Hspg2-/- -Tg) mice and control (WT-Tg) mice.
  • Assessed white adipose tissue mass, cell size, lipid deposition, and energy source utilization.
  • Analyzed insulin sensitivity, skeletal muscle fiber composition, mitochondrial content, and PGC1α protein levels.

Main Results:

  • Hspg2-/- -Tg mice exhibited reduced white adipose tissue mass and cell size.
  • These mice showed no abnormal lipid deposition (e.g., fatty liver) and increased fat consumption via enhanced fatty acid oxidation.
  • Increased insulin sensitivity, elevated muscle type IIA (oxidative) fibers, greater mitochondrial quantity, and higher PGC1α levels were observed in perlecan-deficient mice.

Conclusions:

  • Perlecan may function as a mechano-regulator of lipid and glucose catabolism by promoting oxidative muscle fibers.
  • Downregulation of perlecan presents a potential therapeutic strategy for managing metabolic syndrome and obesity.

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