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The role of adipose tissue dysfunction in hepatic insulin resistance and T2D.

J. Endocrinol. 262:e240115 (2024)
Verlagsversion DOI PMC
Open Access Hybrid
Creative Commons Lizenzvertrag
The root cause of type 2 diabetes (T2D) is insulin resistance (IR), defined by the failure of cells to respond to circulating insulin to maintain lipid and glucose homeostasis. While the causes of whole-body insulin resistance are multifactorial, a major contributing factor is dysregulation of liver and adipose tissue function. Adipose dysfunction, particularly adipose tissue-IR (adipo-IR), plays a crucial role in the development of hepatic insulin resistance and the progression of metabolic dysfunction-associated steatotic liver disease (MASLD) in the context of T2D. In this review, we will focus on molecular mechanisms of hepatic insulin resistance and its association with adipose tissue function. A deeper understanding of the pathophysiological mechanisms of the transition from a healthy state to insulin resistance, impaired glucose tolerance, and T2D may enable us to prevent and intervene in the progression to T2D.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter Adipose Tissue ; Insulin Resistance ; Masld ; Type 2 Diabetes; Extracellular Vesicles; Glucose-production; Gene-expression; Phosphoinositide 3-kinase; Glycogen-synthesis; Induced Lipokine; Low-carbohydrate; Mice Lacking; Fat Diet; Liver
Sprache englisch
Veröffentlichungsjahr 2024
HGF-Berichtsjahr 2024
ISSN (print) / ISBN 0022-0795
e-ISSN 1479-6805
Quellenangaben Band: 262, Heft: 3, Seiten: , Artikelnummer: e240115 Supplement: ,
Verlag Society for Endocrinology
Verlagsort Starling House, 1600 Bristol Parkway N, Bristol, England
Begutachtungsstatus Peer reviewed
POF Topic(s) 90000 - German Center for Diabetes Research
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-502400-001
Förderungen German Center for Diabetes Research (DZD e.V.)
German Federal Ministry for Education and Research
Scopus ID 85200620827
PubMed ID 38967989
Erfassungsdatum 2024-09-04