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 ...
    • Immune Environment in Glioblastoma (Feb 2023)
    • Korsmeyer Award 25th Anniversary Collection (Jan 2023)
    • Aging (Jul 2022)
    • Next-Generation Sequencing in Medicine (Jun 2022)
    • New Therapeutic Targets in Cardiovascular Diseases (Mar 2022)
    • Immunometabolism (Jan 2022)
    • Circadian Rhythm (Oct 2021)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Commentaries
    • Research letters
    • Letters to the editor
    • 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
  • Research letters
  • Letters to the editor
  • 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
  • Abstract
  • Version history
  • Article usage
  • Citations to this article

Advertisement

Research Article Free access | 10.1172/JCI118727

Essentiality of circulating fatty acids for glucose-stimulated insulin secretion in the fasted rat.

D T Stein, V Esser, B E Stevenson, K E Lane, J H Whiteside, M B Daniels, S Chen, and J D McGarry

Department of Internal Medicine, Gifford Laboratories, University of Texas Southwestern Medical Center at Dallas 75235, USA.

Find articles by Stein, D. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, Gifford Laboratories, University of Texas Southwestern Medical Center at Dallas 75235, USA.

Find articles by Esser, V. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, Gifford Laboratories, University of Texas Southwestern Medical Center at Dallas 75235, USA.

Find articles by Stevenson, B. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, Gifford Laboratories, University of Texas Southwestern Medical Center at Dallas 75235, USA.

Find articles by Lane, K. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, Gifford Laboratories, University of Texas Southwestern Medical Center at Dallas 75235, USA.

Find articles by Whiteside, J. in: JCI | PubMed | Google Scholar

Department of Internal Medicine, Gifford Laboratories, University of Texas Southwestern Medical Center at Dallas 75235, USA.

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

Department of Internal Medicine, Gifford Laboratories, University of Texas Southwestern Medical Center at Dallas 75235, USA.

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

Department of Internal Medicine, Gifford Laboratories, University of Texas Southwestern Medical Center at Dallas 75235, USA.

Find articles by McGarry, J. in: JCI | PubMed | Google Scholar

Published June 15, 1996 - More info

Published in Volume 97, Issue 12 on June 15, 1996
J Clin Invest. 1996;97(12):2728–2735. https://doi.org/10.1172/JCI118727.
© 1996 The American Society for Clinical Investigation
Published June 15, 1996 - Version history
View PDF
Abstract

We asked whether the well known starvation-induced impairment of glucose-stimulated insulin secretion (GSIS) seen in isolated rat pancreas preparations also applies in vivo. Accordingly, fed and 18-24-h-fasted rats were subjected to an intravenous glucose challenge followed by a hyperglycemic clamp protocol, during which the plasma-insulin concentration was measured. Surprisingly, the acute (5 min) insulin response was equally robust in the two groups. However, after infusion of the antilipolytic agent, nicotinic acid, to ensure low levels of plasma FFA before the glucose load, GSIS was essentially ablated in fasted rats, but unaffected in fed animals. Maintenance of a high plasma FFA concentration by coadministration of Intralipid plus heparin to nicotinic acid-treated rats (fed or fasted), or further elevation of the endogenous FFA level in nonnicotinic acid-treated fasted animals by infusion of etomoxir (to block hepatic fatty acid oxidation), resulted in supranormal GSIS. The in vivo findings were reproduced in studies with the perfused pancreas from fed and fasted rats in which GSIS was examined in the absence and presence of palmitate. The results establish that in the rat, the high circulating concentration of FFA that accompanies food deprivation is a sine qua non for efficient GSIS when a fast is terminated. They also serve to underscore the powerful interaction between glucose and fatty acids in normal beta cell function and raise the possibility that imbalances between the two fuels in vivo could have pathological consequences.

Version history
  • Version 1 (June 15, 1996): 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
  • Abstract
  • Version history
Advertisement
Advertisement

Copyright © 2023 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts