Characterization of signal transduction and glucose transport in skeletal muscle from type 2 diabetic patients

↓ Direkt till sidans innehåll
↓ Direkt till sidans sekundära innehåll (sidomenyn)

Search: id:"swepub:oai:prod.swepub.kib.ki.se:1941495" > Characterization of...

1 of 1
Previous record
Next record
To hitlist

Details
MARC

Krook, AKarolinska Institutet (author)

Characterization of signal transduction and glucose transport in skeletal muscle from type 2 diabetic patients

Article/chapterEnglish2000

Publisher, publication year, extent ...

American Diabetes Association,2000

Numbers

LIBRIS-ID:oai:prod.swepub.kib.ki.se:1941495
http://kipublications.ki.se/Default.aspx?queryparsed=id:1941495URI
https://doi.org/10.2337/diabetes.49.2.284DOI

Supplementary language notes

Language:English
Summary in:English

Part of subdatabase

SwePubSwePub

Classification

Subject category:ref swepub-contenttype
Subject category:art swepub-publicationtype

Notes

We characterized metabolic and mitogenic signaling pathways in isolated skeletal muscle from well-matched type 2 diabetic and control subjects. Time course studies of the insulin receptor, insulin receptor substrate (IRS)-1/2, and phosphatidylinositol (PI) 3-kinase revealed that signal transduction through this pathway was engaged between 4 and 40 min. Insulin-stimulated (0.6-60 nmol/l) tyrosine phosphorylation of the insulin receptor beta-subunit, mitogen-activated protein (MAP) kinase phosphorylation, and glycogen synthase activity were not altered in type 2 diabetic subjects. In contrast, insulin-stimulated tyrosine phosphorylation of IRS-1 and anti-phosphotyrosine-associated PI 3-kinase activity were reduced 40-55% in type 2 diabetic subjects at high insulin concentrations (2.4 and 60 nmol/l, respectively). Impaired glucose transport activity was noted at all insulin concentrations (0.6-60 nmol/l). Aberrant protein expression cannot account for these insulin-signaling defects because expression of insulin receptor, IRS-1, IRS-2, MAP kinase, or glycogen synthase was similar between type 2 diabetic and control subjects. In skeletal muscle from type 2 diabetic subjects, IRS-1 phosphorylation, PI 3-kinase activity, and glucose transport activity were impaired, whereas insulin receptor tyrosine phosphorylation, MAP kinase phosphorylation, and glycogen synthase activity were normal. Impaired insulin signal transduction in skeletal muscle from type 2 diabetic patients may partly account for reduced insulin-stimulated glucose transport; however, additional defects are likely to play a role.

Added entries (persons, corporate bodies, meetings, titles ...)

Bjornholm, MKarolinska Institutet (author)
Galuska, DKarolinska Institutet (author)
Jiang, XJ (author)
Fahlman, R (author)
Myers, MG (author)
Wallberg-Henriksson, HKarolinska Institutet (author)
Zierath, JRKarolinska Institutet (author)
Karolinska Institutet (creator_code:org_t)

Related titles

In:Diabetes: American Diabetes Association49:2, s. 284-2920012-17971939-327X

Internet link

Find in a library

Diabetes (Search for host publication in LIBRIS)

To the university's database

1 of 1
Previous record
Next record
To hitlist

Find more in SwePub

By the author/editor: Krook, A; Bjornholm, M; Galuska, D; Jiang, XJ; Fahlman, R; Myers, MG; show more...; Wallberg-Henriks ...; Zierath, JR; show less...

Articles in the publication: Diabetes

By the university: Karolinska Institutet

Search outside SwePub

Extend your search to:: Google; Google Book Search; Google Scholar

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

LIBRIS.kb.se