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image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Medical Clinics of N...arrow_drop_down
image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao
Medical Clinics of North America
Article . 2004 . Peer-reviewed
License: Elsevier TDM
Data sources: Crossref
image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao
https://doi.org/10.1007/978-3-...
Part of book or chapter of book . 2018 . Peer-reviewed
License: Springer TDM
Data sources: Crossref
image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao
https://doi.org/10.1007/978-3-...
Part of book or chapter of book . 2018 . Peer-reviewed
License: Springer TDM
Data sources: Crossref
Medical Clinics of North America
Article . 2004
Data sources: Europe PubMed Central
Medical Clinics of North America
Article
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Pathogenesis of type 2 diabetes mellitus

descriptionPublicationkeyboard_double_arrow_right Article , Part of book or chapter of book 01 Jul 2004 English Publisher:Elsevier BVJournal:Medical Clinics of North America, volume 88, pages 787-835 (issn: 0025-7125, Copyright policy )
Authors: Ralph A. DeFronzo;

doi: 10.1016/j.mcna.2004.04.013 , 10.1007/978-3-319-45015-5_8 , 10.1007/978-3-319-27317-4_8-1

pmid: 15308380

Pathogenesis of type 2 diabetes mellitus

Abstract

This article provides an overview of the pathogenesis of type 2 diabetes mellitus. Discussion begins by describing normal glucose homeostasis and ingestion of a typical meal and then discusses glucose homeostasis in diabetes. Topics covered include insulin secretion in type 2 diabetes mellitus and insulin resistance, the site of insulin resistance, the interaction between insulin sensitivity and secretion, the role of adipocytes in the pathogenesis of type 2 diabetes, cellular mechanisms of insulin resistance including glucose transport and phosphorylation, glycogen and synthesis,glucose and oxidation, glycolysis, and insulin signaling.

Related Organizations
Keywords

Blood Glucose, Male, Prognosis, Severity of Illness Index, Diabetes Mellitus, Type 2, Risk Factors, Glucose Intolerance, Insulin Secretion, Humans, Hypoglycemic Agents, Insulin, Female, Insulin Resistance, Phosphorylation

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citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
1K
Top 0.1%
Top 0.1%
Top 1%
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