A signal for β-cell failure

Joseph Avruch ()
Additional contact information
Joseph Avruch: Diabetes Unit, Massachusetts General Hospital and Harvard Medical School

Nature, 1998, vol. 391, issue 6670, 846-847

Abstract: A hallmark of human type 2 diabetes is hyperglycaemia — an excess of glucose in the bloodstream. Normally, the pancreatic β-cell compensate for this by secreting more insulin, but this fail-safe mechanism seems to malfunction in patients with the condition. Now, by generating mice that lack the insulin-receptor substrate-2 (IRS-2) gene, one group has shown that IRS-2 may be responsible for both increased insulin resistance and reduced insulin compenation. The knockout mice develop a syndrome that closely resembles human type 2 diabetes and, importantly, they have fewer β-cells than wild-type mice.

Date: 1998
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/35998 Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:391:y:1998:i:6670:d:10.1038_35998

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/35998

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().