Role of caveolin and caveolae in insulin signaling and diabetes

Alex W. Cohen, Terry P. Combs, Philipp E. Scherer, Michael P. Lisanti

Research output: Contribution to journalArticle

163 Citations (Scopus)

Abstract

Caveolae are specialized membrane microdomains present within the plasma membrane of the vast majority of cell types. They have a unique composition in that they are highly enriched in cholesterol, sphingolipids, and their coat proteins the caveolins (-1, -2, and -3). In recent years it has been recognized that caveolae act as signaling platforms, serving as a concentrating point for numerous signaling molecules, as well as regulating flux through many distinct signaling cascades. Although caveolae are found in a variety of cell types, they are most abundant in adipose tissue. This fact has led to the intense study of the function of these organelles in adipocytes. It has now become apparent that effective insulin signaling in the adipocyte may be strictly dependent on localization of at least two insulin-responsive elements to caveolae (insulin receptor and GLUT4), as well as on a direct functional interaction between caveolin-1 and the insulin receptor. We present a critical discussion of these recent findings.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume285
Issue number6 48-6
StatePublished - Dec 2003

Fingerprint

Caveolins
Caveolae
Medical problems
Insulin
Caveolin 1
Insulin Receptor
Adipocytes
Caveolin 2
Membrane Microdomains
Sphingolipids
Capsid Proteins
Cell membranes
Organelles
Adipose Tissue
Cholesterol
Cell Membrane
Tissue
Fluxes
Membranes
Molecules

Keywords

  • Caveolin-1
  • Glucose transporter 4
  • Insulin receptor

ASJC Scopus subject areas

  • Physiology
  • Endocrinology
  • Biochemistry

Cite this

Role of caveolin and caveolae in insulin signaling and diabetes. / Cohen, Alex W.; Combs, Terry P.; Scherer, Philipp E.; Lisanti, Michael P.

In: American Journal of Physiology - Endocrinology and Metabolism, Vol. 285, No. 6 48-6, 12.2003.

Research output: Contribution to journalArticle

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