Home LiteratureArticle Details
PMID: 46056 Published · ppublish English Journal Article

Mode of insulin action.

Lancet (London, England) ·Vol. 1 ·No. 7899 ·1975-01-18 ·Pages 144-7

Kissebah AH, Tulloch BR, Hope-Gill H, Clarke PV, Vydelingum N, Fraser TR

Abstract

A unifying hypothesis is proposed for the mechanism of insulin action in adipose tissue. Insulin both induces displacement of Ca++ from a membrane-bound pool and inhibits efflux of the ion, thereby facilitating a rise in intracellular free Ca++ concentration. The former effect could enhance the transport of substrates and ions into the cell, while the latter modulates the activity of some intracellular enzymes to stimulate glycogenesis, lipogenesis, and decrease lipolysis and glycogenolysis. The calcium ion might act as the missing second messenger for insulin action.

MeSH Terms
Adenosine Triphosphate/metabolism Adipose Tissue/enzymology,metabolism Animals Binding Sites Biological Transport, Active Calcium/metabolism Cyclic AMP/metabolism Enzyme Activation Humans In Vitro Techniques Insulin/physiology Lipase/metabolism Oxidative Phosphorylation Phosphoproteins/metabolism Phosphoric Monoester Hydrolases/metabolism Protein Kinases/metabolism Rats Triglycerides/metabolism
Chemicals
Insulin Phosphoproteins Triglycerides Adenosine Triphosphate Cyclic AMP Protein Kinases Lipase Phosphoric Monoester Hydrolases Calcium
Authors & Affiliations
6 authors, click to expand affiliations / ORCID
Kissebah A H
Tulloch B R
Hope-Gill H
Clarke P V
Vydelingum N
Fraser T R
Article Info
Journal
Lancet (London, England)
Abbr.
Lancet
ISSN
0140-6736
Published
1975-01-18
Pages
144-7
Language
English
Region
England
NLM ID
2985213R
Subset
IM
Analysis Services
Analysis Services

Contact

No. 2 Wenbo Road, Zhangqiu District, Jinan, Shandong

Qilu Normal University · Genelibs Bioinformatics Lab

750 Shunhua Rd, Jinan

2F, Bldg F, University Science Park

Tel: 0531-88819269

WeChat Official Account

Follow our WeChat subscription account for real-time updates and the latest in medical and biological research.


Business Email

E-mail: [email protected]