Elevated PC-1 content in cultured skin fibroblasts correlates with decreased in vivo and in vitro insulin action in nondiabetic subjects: Evidence that PC-1 may be an intrinsic factor in impaired insulin receptor signaling

Lucia Frittitta, Daniela Spampinato, Anna Solini, Romano Nosadini, Ira D. Goldfine, Riccardo Vigneri, Vincenzo Trischitta

Research output: Contribution to journalArticlepeer-review

Abstract

Membrane glycoprotein PC-1 inhibits insulin receptor (IR) tyrosine kinase activity and subsequent cellular signaling. PC-1 content is elevated in muscle and adipose tissue from insulin-resistant subjects, and its elevation correlates with in vivo insulin resistance. To determine whether elevated PC-I content is a primary cause of insulin resistance, we have now measured PC-1 content in cultured skin fibroblasts from nonobese nondiabetic insulin-resistant subjects and found that 1) PC-1 content was significantly higher in these cells when compared with cells from insulin-sensitive subjects (6.7 ± 0.9 vs. 3.1 ± 0.6 ng/0.1 mg protein, mean ± SE, P <0.01); 2) PC-1 content in fibroblasts was highly correlated with PC-1 content in muscle tissue (r = 0.95, P = 0.01); 3) PC-1 content in fibroblasts negatively correlated with both decreased in vivo insulin sensitivity and decreased in vitro IR autophosphorylation; and 4) in cells from insulin-resistant subjects, insulin stimulation of glycogen synthetase was decreased. These studies indicate, therefore, that the elevation of PC-1 content may be a primary factor in the cause of insulin resistance.

Original languageEnglish
Pages (from-to)1095-1100
Number of pages6
JournalDiabetes
Volume47
Issue number7
DOIs
Publication statusPublished - 1998

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Fingerprint Dive into the research topics of 'Elevated PC-1 content in cultured skin fibroblasts correlates with decreased in vivo and in vitro insulin action in nondiabetic subjects: Evidence that PC-1 may be an intrinsic factor in impaired insulin receptor signaling'. Together they form a unique fingerprint.

Cite this