Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
  • Current issue
  • Past issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Author's Takes
  • Reviews
    • View all reviews ...
    • Aging (Upcoming)
    • Next-Generation Sequencing in Medicine (Jun 2022)
    • New Therapeutic Targets in Cardiovascular Diseases (Mar 2022)
    • Immunometabolism (Jan 2022)
    • Circadian Rhythm (Oct 2021)
    • Gut-Brain Axis (Jul 2021)
    • Tumor Microenvironment (Mar 2021)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Commentaries
    • Concise Communication
    • Editorials
    • Viewpoint
    • Top read articles
  • Clinical Medicine
  • JCI This Month
    • Current issue
    • Past issues

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Author's Takes
  • In-Press Preview
  • Commentaries
  • Concise Communication
  • Editorials
  • Viewpoint
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
Top
  • View PDF
  • Download citation information
  • Send a comment
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal
  • Top
  • Version history
  • Article usage
  • Citations to this article

Advertisement

CorrigendumMetabolism Free access | 10.1172/JCI31408C1

Muscle-specific knockout of PKC-λ impairs glucose transport and induces metabolic and diabetic syndromes

Robert V. Farese, Mini P. Sajan, Hong Yang, Pengfei Li, Steven Mastorides, William R. Gower Jr., Sonali Nimal, Cheol Soo Choi, Sheene Kim, Gerald I. Shulman, C. Ronald Kahn, Ursula Braun, and Michael Leitges

Find articles by Farese, R. in: JCI | PubMed | Google Scholar

Find articles by Sajan, M. in: JCI | PubMed | Google Scholar

Find articles by Yang, H. in: JCI | PubMed | Google Scholar

Find articles by Li, P. in: JCI | PubMed | Google Scholar

Find articles by Mastorides, S. in: JCI | PubMed | Google Scholar

Find articles by Gower, W. in: JCI | PubMed | Google Scholar

Find articles by Nimal, S. in: JCI | PubMed | Google Scholar

Find articles by Choi, C. in: JCI | PubMed | Google Scholar

Find articles by Kim, S. in: JCI | PubMed | Google Scholar

Find articles by Shulman, G. in: JCI | PubMed | Google Scholar

Find articles by Kahn, C. in: JCI | PubMed | Google Scholar

Find articles by Braun, U. in: JCI | PubMed | Google Scholar

Find articles by Leitges, M. in: JCI | PubMed | Google Scholar

Published October 1, 2007 - More info

Published in Volume 117, Issue 10 on October 1, 2007
J Clin Invest. 2007;117(10):3141–3141. https://doi.org/10.1172/JCI31408C1.
© 2007 The American Society for Clinical Investigation
Published October 1, 2007 - Version history
View PDF

Related article:

Muscle-specific knockout of PKC-λ impairs glucose transport and induces metabolic and diabetic syndromes
Robert V. Farese, … , Ursula Braun, Michael Leitges
Robert V. Farese, … , Ursula Braun, Michael Leitges
Research Article Metabolism

Muscle-specific knockout of PKC-λ impairs glucose transport and induces metabolic and diabetic syndromes

  • Text
  • PDF
Abstract

Obesity, the metabolic syndrome, and type 2 diabetes mellitus (T2DM) are major global health problems. Insulin resistance is frequently present in these disorders, but the causes and effects of such resistance are unknown. Here, we generated mice with muscle-specific knockout of the major murine atypical PKC (aPKC), PKC-λ, a postulated mediator for insulin-stimulated glucose transport. Glucose transport and translocation of glucose transporter 4 (GLUT4) to the plasma membrane were diminished in muscles of both homozygous and heterozygous PKC-λ knockout mice and were accompanied by systemic insulin resistance; impaired glucose tolerance or diabetes; islet β cell hyperplasia; abdominal adiposity; hepatosteatosis; elevated serum triglycerides, FFAs, and LDL-cholesterol; and diminished HDL-cholesterol. In contrast to the defective activation of muscle aPKC, insulin signaling and actions were intact in muscle, liver, and adipocytes. These findings demonstrate the importance of aPKC in insulin-stimulated glucose transport in muscles of intact mice and show that insulin resistance and resultant hyperinsulinemia owing to a specific defect in muscle aPKC is sufficient to induce abdominal obesity and other lipid abnormalities of the metabolic syndrome and T2DM. These findings are particularly relevant because humans who have obesity, impaired glucose tolerance, and T2DM reportedly have defective activation and/or diminished levels of muscle aPKC.

Authors

Robert V. Farese, Mini P. Sajan, Hong Yang, Pengfei Li, Steven Mastorides, William R. Gower Jr., Sonali Nimal, Cheol Soo Choi, Sheene Kim, Gerald I. Shulman, C. Ronald Kahn, Ursula Braun, Michael Leitges

×

Original citation: J. Clin. Invest.117:2289-2301 (2007). doi:10.1172/JCI31408.

Citation for this corrigendum: J. Clin. Invest.117:3141 (2007). doi:10.1172/JCI31408C1.

In the original version of the manuscript, lanes in the gels in Figure 4, bottom panel, were shifted to align with the other presentations of the histograms. This introduced inconsistencies into the blots. The original unaltered blots are shown below, with the histograms accordingly adjusted.

The authors regret the error.

Version history
  • Version 1 (October 1, 2007): No description

Article tools

  • View PDF
  • Download citation information
  • Send a comment
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal

Metrics

  • Article usage
  • Citations to this article

Go to

  • Top
  • Version history
Advertisement
Advertisement

Copyright © 2022 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts