TY - JOUR
T1 - Beyond adiponectin and leptin
T2 - Adipose tissue-derived mediators of inter-organ communication
AU - Funcke, Jan Bernd
AU - Scherer, Philipp E.
N1 - Funding Information:
This work was supported by Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) Grant 414232833 (J-B.F.); National Institute of Diabetes and Digestive and Kidney Diseases Grants R01-DK55758, P01-DK088761, and R01-DK099110 (P.E.S.); National Institute on Aging Grant P01-AG051459 (P.E.S.); and an unrestricted grant from the Novo Nordisk Research Foundation (P.E.S.). Manuscript received 19 March 2019 and in revised form 17 June 2019. Published, JLR Papers in Press, June 17, 2019 DOI https://doi.org/10.1194/jlr.R094060
Publisher Copyright:
Copyright © 2019 Funcke and Scherer.
PY - 2019
Y1 - 2019
N2 - The breakthrough discoveries of leptin and adiponectin more than two decades ago led to a widespread recognition of adipose tissue as an endocrine organ. Many more adipose tissue-secreted signaling mediators (adipokines) have been identified since then, and much has been learned about how adipose tissue communicates with other organs of the body to maintain systemic homeostasis. Beyond proteins, additional factors, such as lipids, metabolites, noncoding RNAs, and extracellular vesicles (EVs), released by adipose tissue participate in this process. Here, we review the diverse signaling mediators and mechanisms adipose tissue utilizes to relay information to other organs. We discuss recently identified adipokines (proteins, lipids, and metabolites) and briefly outline the contributions of noncoding RNAs and EVs to the ever-increasing complexities of adipose tissue inter-organ communication. We conclude by reflecting on central aspects of adipokine biology, namely, the contribution of distinct adipose tissue depots and cell types to adipokine secretion, the phenomenon of adipokine resistance, and the capacity of adipose tissue to act both as a source and sink of signaling mediators.
AB - The breakthrough discoveries of leptin and adiponectin more than two decades ago led to a widespread recognition of adipose tissue as an endocrine organ. Many more adipose tissue-secreted signaling mediators (adipokines) have been identified since then, and much has been learned about how adipose tissue communicates with other organs of the body to maintain systemic homeostasis. Beyond proteins, additional factors, such as lipids, metabolites, noncoding RNAs, and extracellular vesicles (EVs), released by adipose tissue participate in this process. Here, we review the diverse signaling mediators and mechanisms adipose tissue utilizes to relay information to other organs. We discuss recently identified adipokines (proteins, lipids, and metabolites) and briefly outline the contributions of noncoding RNAs and EVs to the ever-increasing complexities of adipose tissue inter-organ communication. We conclude by reflecting on central aspects of adipokine biology, namely, the contribution of distinct adipose tissue depots and cell types to adipokine secretion, the phenomenon of adipokine resistance, and the capacity of adipose tissue to act both as a source and sink of signaling mediators.
KW - Angiopoietin
KW - Angiopoietin-like protein
KW - Bone morphogenic protein
KW - Chemerin
KW - Endotrophin
KW - Extracellular vesicles
KW - Fatty acid esters of hydroxy fatty acids
KW - Fibroblast growth factor 21
KW - Lipocalin 2
KW - Long noncoding ribonucleic acids
KW - Lysophosphatidic acids
KW - Micro-ribonucleic acids
KW - Neuregulin 4
KW - Sphingolipids
KW - Uric acid
KW - Uridine
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U2 - 10.1194/jlr.R094060
DO - 10.1194/jlr.R094060
M3 - Review article
C2 - 31209153
AN - SCOPUS:85072820506
SN - 0022-2275
VL - 60
SP - 1648
EP - 1697
JO - Journal of lipid research
JF - Journal of lipid research
IS - 10
ER -