Deletion of Cavin/PTRF Causes Global Loss of Caveolae, Dyslipidemia, and Glucose Intolerance

Libin Liu, Dennis Brown, Mary McKee, Nathan K. LeBrasseur, Dan Yang, Kenneth H. Albrecht, Katya Ravid, Paul F. Pilch

Research output: Contribution to journalArticle

235 Scopus citations

Abstract

Caveolae are specialized invaginations of the plasma membrane found in numerous cell types. They have been implicated as playing a role in a variety of physiological processes and are typically characterized by their association with the caveolin family of proteins. We show here by means of targeted gene disruption in mice that a distinct caveolae-associated protein, Cavin/PTRF, is an essential component of caveolae. Animals lacking Cavin have no morphologically detectable caveolae in any cell type examined and have markedly diminished protein expression of all three caveolin isoforms while retaining normal or above normal caveolin mRNA expression. Cavin-knockout mice are viable and of normal weight but have higher circulating triglyceride levels, significantly reduced adipose tissue mass, glucose intolerance, and hyperinsulinemia-characteristics that constitute a lipodystrophic phenotype. Our results underscore the multiorgan role of caveolae in metabolic regulation and the obligate presence of Cavin for caveolae formation.

Original languageEnglish (US)
Pages (from-to)310-317
Number of pages8
JournalCell Metabolism
Volume8
Issue number4
DOIs
StatePublished - Oct 8 2008

Keywords

  • HUMDISEASE
  • SIGNALING

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Cell Biology

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