PTRF acts as an adipokine contributing to adipocyte dysfunctionality and ectopic lipid deposition
Resumen: Adipose tissue (AT) expands under obesogenic conditions. Yet, when the growth exceeds a certain limit, AT becomes dysfunctional and surplus lipids start depositing ectopically. Polymerase I and transcription release factor (PTRF) has been proposed as a mechanism leading to a dysfunctional AT by decreasing the adipogenic potential of human adipocyte precursors. However, whether or not PTRF can be secreted by the adipocytes into the bloodstream is not yet known. For this work, PTRF presence was investigated in plasma. We also produced a recombinant PTRF (rPTRF) and examined its impact on the functional interactions between the adipocyte and the hepatocyte in vitro. We demonstrated that PTRF can be found in human plasma, and is at least in part, carried by exosomes. In vitro treatment with rPTRF increased the hypertrophy and senescence of 3T3-L1 adipocytes. In turn, those rPTRF-treated adipocytes increased lipid accumulation in hepatocytes. Lastly, we found a positive correlation between circulating PTRF and the concentration of PTRF in the visceral fat depot. All these findings point toward the presence of an enlarged and dysfunctional visceral adipose tissue which secretes PTRF. This circulating PTRF behaves as an adipokine and may partially contribute to the well-known detrimental effects of visceral fat accumulation.
Idioma: Inglés
DOI: 10.1007/s13105-018-0638-9
Año: 2018
Publicado en: Journal of Physiology and Biochemistry 74, 4 (2018), 613-622
ISSN: 1138-7548

Factor impacto JCR: 2.523 (2018)
Categ. JCR: PHYSIOLOGY rank: 38 / 81 = 0.469 (2018) - Q2 - T2
Categ. JCR: BIOCHEMISTRY & MOLECULAR BIOLOGY rank: 169 / 294 = 0.575 (2018) - Q3 - T2

Factor impacto SCIMAGO: 0.872 - Biochemistry (Q2) - Physiology (Q2) - Medicine (miscellaneous) (Q2)

Financiación: info:eu-repo/grantAgreement/ES/FEDER/Una manera de hacer Europa
Tipo y forma: Article (PostPrint)

Rights Reserved All rights reserved by journal editor

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 Record created 2019-06-07, last modified 2020-01-17

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