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Nono Nankam, P.A. ; Blüher, M.

Retinol-binding protein 4 in obesity and metabolic dysfunctions.

Mol. Cell. Endocrinol. 531:111312 (2021)
Verlagsversion DOI PMC
Open Access Gold (Paid Option)
Creative Commons Lizenzvertrag
Excessive increased adipose tissue mass in obesity is associated with numerous co-morbid disorders including increased risk of type 2 diabetes, fatty liver disease, hypertension, dyslipidemia, cardiovascular diseases, dementia, airway disease and some cancers. The causal mechanisms explaining these associations are not fully understood. Adipose tissue is an active endocrine organ that secretes many adipokines, cytokines and releases metabolites. These biomolecules referred to as adipocytokines play a significant role in the regulation of whole-body energy homeostasis and metabolism by influencing and altering target tissues function. Understanding the mechanisms of adipocytokine actions represents a hot topic in obesity research. Among several secreted bioactive signalling molecules from adipose tissue and liver, retinol-binding protein 4 (RBP4) has been associated with systemic insulin resistance, dyslipidemia, type 2 diabetes and other metabolic diseases. Here, we aim to review and discuss the current knowledge on RBP4 with a focus on its role in the pathogenesis of obesity comorbid diseases.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Korrespondenzautor
Schlagwörter Adipocytokines ; Adipose Tissue ; Insulin Resistance ; Metabolic Risks ; Obesity; Fatty Liver-disease; Adipose-tissue Dysfunction; Type-2 Diabetes-mellitus; Insulin-resistance; Serum Retinol; Vitamin-a; Body-fat; Macular Degeneration; Rbp4 Levels; Weight-loss
ISSN (print) / ISBN 0303-7207
e-ISSN 1872-8057
Zeitschrift Molecular and Cellular Endocrinology
Quellenangaben Band: 531, Heft: , Seiten: , Artikelnummer: 111312 Supplement: ,
Verlag Elsevier
Verlagsort Shannon
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG)
Förderungen Deutsche Forschungsgemeinschaft (DFG) , Germany