Mechanism of Insulin Resistance Induced by Sustained Levels of Cytosolic Free Calcium in Rat Adipocytes* (original) (raw)

Journal Article

,

1

Research Service and the Department of Medicine, Veterans Administration Medical Center

Denver, Colorado 80220

;

The Department of Medicine, Indiana University Medical Center and Veterans Administration Hospital

Indianapolis, Indiana 46202

;

The Section on Molecular and Cellular Physiology, Diabetes Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health

Bethesda, Maryland 20892

Search for other works by this author on:

,

1

Research Service and the Department of Medicine, Veterans Administration Medical Center

Denver, Colorado 80220

;

The Department of Medicine, Indiana University Medical Center and Veterans Administration Hospital

Indianapolis, Indiana 46202

;

The Section on Molecular and Cellular Physiology, Diabetes Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health

Bethesda, Maryland 20892

Search for other works by this author on:

,

1

Research Service and the Department of Medicine, Veterans Administration Medical Center

Denver, Colorado 80220

;

The Department of Medicine, Indiana University Medical Center and Veterans Administration Hospital

Indianapolis, Indiana 46202

;

The Section on Molecular and Cellular Physiology, Diabetes Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health

Bethesda, Maryland 20892

Search for other works by this author on:

,

1

Research Service and the Department of Medicine, Veterans Administration Medical Center

Denver, Colorado 80220

;

The Department of Medicine, Indiana University Medical Center and Veterans Administration Hospital

Indianapolis, Indiana 46202

;

The Section on Molecular and Cellular Physiology, Diabetes Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health

Bethesda, Maryland 20892

Search for other works by this author on:

,

1

Research Service and the Department of Medicine, Veterans Administration Medical Center

Denver, Colorado 80220

;

The Department of Medicine, Indiana University Medical Center and Veterans Administration Hospital

Indianapolis, Indiana 46202

;

The Section on Molecular and Cellular Physiology, Diabetes Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health

Bethesda, Maryland 20892

Search for other works by this author on:

,

1

Research Service and the Department of Medicine, Veterans Administration Medical Center

Denver, Colorado 80220

;

The Department of Medicine, Indiana University Medical Center and Veterans Administration Hospital

Indianapolis, Indiana 46202

;

The Section on Molecular and Cellular Physiology, Diabetes Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health

Bethesda, Maryland 20892

Search for other works by this author on:

,

1

Research Service and the Department of Medicine, Veterans Administration Medical Center

Denver, Colorado 80220

;

The Department of Medicine, Indiana University Medical Center and Veterans Administration Hospital

Indianapolis, Indiana 46202

;

The Section on Molecular and Cellular Physiology, Diabetes Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health

Bethesda, Maryland 20892

Search for other works by this author on:

1

Research Service and the Department of Medicine, Veterans Administration Medical Center

Denver, Colorado 80220

;

The Department of Medicine, Indiana University Medical Center and Veterans Administration Hospital

Indianapolis, Indiana 46202

;

The Section on Molecular and Cellular Physiology, Diabetes Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health

Bethesda, Maryland 20892

Search for other works by this author on:

Published:

01 November 1989

• • Article contents
  • Figures & tables
  • Video
  • Audio
  • Supplementary Data
• Cite

Cite

BORIS DRAZNIN, DAVID LEWIS, NANCY HOULDER, NANCY SHERMAN, MARTIN ADAMO, W. TIMOTHY GARVEY, DEREK LEROITH, KARL SUSSMAN, Mechanism of Insulin Resistance Induced by Sustained Levels of Cytosolic Free Calcium in Rat Adipocytes, Endocrinology, Volume 125, Issue 5, 1 November 1989, Pages 2341–2349, https://doi.org/10.1210/endo-125-5-2341
Close

Navbar Search Filter Mobile Enter search term Search

Abstract

We have recently provided evidence that elevated levels of cytosolic free Ca2+ ([Ca2+]i) decreased insulinstimulated glucose uptake in isolated rat adipocytes. To investigate the mechanism of Ca2+ action, we examined the effects of elevated levels of [Ca2+]i on insulin binding, autophosphorylation, and tyrosine kinase activity (TKA) of insulin receptors as well as basal and insulin-stimulated cellular distribution of glucose transporters. The latter was assessed by cytochalasin-B binding to plasma membrane and cytosolic fractions. Elevated concentrations of [Ca2+]i were maintained by incubating adipocytes with a depolarizing concentration of K+ (40 mM). Basal nonstimulated glucose uptake was not altered by increased levels of [Ca2+]i. Adipocytes with higher [Ca2+]i (220 ± 15 nM) showed 30% reduction in insulin-stimulated 2-deoxyglucose uptake compared with control cells ([Ca2+]i, 140 ± 18 nM). Moreover, adipocytes with higher levels of [Ca2+]i demonstrated an approximately 10% reduction in autophosphorylation and TKA of insulin receptors without a change in insulin binding. Both basal and insulin-stimulated distributions of glucose transporters were unaffected by sustained levels of [Ca2+]i. The effects of elevated [Ca2+]i were not mimicked by protein kinase-C activation. These observations suggest that 1) elevated or sustained levels of [Ca2+]i impair insulin-stimulated glucose uptake; and 2) Ca2+-induced impairment appears to reside at the postbinding steps of insulin action and probably interferes with the TKA of insulin receptors and the intrinsic activity of glucose transporters.

This content is only available as a PDF.

Copyright © 1989 by The Endocrine Society

You do not currently have access to this article.

Personal account

• Sign in with email/username & password
• Get email alerts
• Save searches
• Purchase content
• Activate your purchase/trial code
• Add your ORCID iD

Get help with access

Institutional access

Access to content on Oxford Academic is often provided through institutional subscriptions and purchases. If you are a member of an institution with an active account, you may be able to access content in one of the following ways:

IP based access

Typically, access is provided across an institutional network to a range of IP addresses. This authentication occurs automatically, and it is not possible to sign out of an IP authenticated account.

Sign in through your institution

Choose this option to get remote access when outside your institution. Shibboleth/Open Athens technology is used to provide single sign-on between your institution’s website and Oxford Academic.

1. Click Sign in through your institution.
2. Select your institution from the list provided, which will take you to your institution's website to sign in.
3. When on the institution site, please use the credentials provided by your institution. Do not use an Oxford Academic personal account.
4. Following successful sign in, you will be returned to Oxford Academic.

If your institution is not listed or you cannot sign in to your institution’s website, please contact your librarian or administrator.

Sign in with a library card

Enter your library card number to sign in. If you cannot sign in, please contact your librarian.

Society Members

Society member access to a journal is achieved in one of the following ways:

Sign in through society site

Many societies offer single sign-on between the society website and Oxford Academic. If you see ‘Sign in through society site’ in the sign in pane within a journal:

1. Click Sign in through society site.
2. When on the society site, please use the credentials provided by that society. Do not use an Oxford Academic personal account.
3. Following successful sign in, you will be returned to Oxford Academic.

If you do not have a society account or have forgotten your username or password, please contact your society.

Sign in using a personal account

Some societies use Oxford Academic personal accounts to provide access to their members. See below.

Personal account

A personal account can be used to get email alerts, save searches, purchase content, and activate subscriptions.

Some societies use Oxford Academic personal accounts to provide access to their members.

Viewing your signed in accounts

Click the account icon in the top right to:

• View your signed in personal account and access account management features.
• View the institutional accounts that are providing access.

Signed in but can't access content

Oxford Academic is home to a wide variety of products. The institutional subscription may not cover the content that you are trying to access. If you believe you should have access to that content, please contact your librarian.

Institutional account management

For librarians and administrators, your personal account also provides access to institutional account management. Here you will find options to view and activate subscriptions, manage institutional settings and access options, access usage statistics, and more.

Purchase

Short-term Access

To purchase short-term access, please sign in to your personal account above.

Don't already have a personal account? Register

Mechanism of Insulin Resistance Induced by Sustained Levels of Cytosolic Free Calcium in Rat Adipocytes* - 24 Hours access

EUR €38.00

GBP £33.00

USD $41.00

Rental

This article is also available for rental through DeepDyve.

Citations

Views

Altmetric

Metrics

Total Views 21

1 Pageviews

20 PDF Downloads

Since 5/1/2017

Citations

105 Web of Science

×

Email alerts

More on this topic

Related articles in PubMed

Citing articles via

• Latest

• Most Read

• Most Cited

More from Oxford Academic