Insulin Action and the Insulin Signaling Network*

Clicks: 3
ID: 303082
1995
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Emerging

Ranked #201 of 220 articles by views in endocrine reviews

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 220 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
IN THE fasted state, glucose homeostasis depends upon the balance between hepatic glucose production and glucose utilization by the major insulin-dependent tissues, such as liver, adipose, and muscle, and by insulin-independent tissues, such as brain and kidney. This balance is tightly regulated by pancreatic hormones. Thus, in normal individuals, the response to increased plasma glucose levels is an increase in secretion of insulin from β-cells of the pancreatic islets. This increase in circulating insulin levels stimulates glucose transport into peripheral tissues and inhibits hepatic gluconeogenesis. In type II diabetes there are at least two fundamental defects: one is a decrease in the ability of peripheral tissues to respond to insulin (insulin resistance), and the second is impaired β-cell function, which results from long-term hyperglycemia. It appears that both genetic and environmental factors are responsible for the progression from normal glucose tolerance to type II diabetes (1–4). In addition to its primary effects on glucose homeostasis, insulin also promotes a number of other cellular events including regulation of ion and amino acid transport, lipid metabolism, glycogen synthesis, gene transcription and mRNA turnover, protein synthesis and degradation, and DNA synthesis (Fig. 1). Thus the actions of insulin play key roles in the normal storage of ingested fuels and in normal cellular growth and differentiation. The biological importance of these effects of insulin are most obvious in the uncontrolled type I diabetic in ketoacidosis (1, 3–5). To fully understand the events leading to insulin-resistant states and the pathophysiology of insulin deficiency, it is necessary to identify, at the molecular level, the key components in the insulin-signaling pathway.
Reference Key
openalex_W2058390591 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Bentley Cheatham, C. Ronald Kahn
Journal endocrine reviews
Year 1995
DOI
10.1210/edrv-16-2-117
URL
https://doi.org/10.1210/edrv-16-2-117
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.