PTRF acts as an adipokine contributing to adipocyte dysfunctionality and ectopic lipid deposition

Pérez-Díaz, Sergio; García-Sobreviela, Maria Pilar; González‐Irazabal, Yolanda; García-Rodríguez, Beatriz; Espina, Silvia; Arenaz, Izaskún; Arbonés-Mainar, José M.

doi:10.1007/s13105-018-0638-9

Cited by 13 publications

(8 citation statements)

References 24 publications

(31 reference statements)

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“…Studies from Perez-Diaz et al further indicated that the plasma exosomal transcription release factor (PTRF) increases the occurrence of hypertrophy and aging of 3 T3-L1 adipocyte hypertrophy and senescence. Circulating polymerase I and PTRF, as adipokines may partially contribute to the deleterious effects of visceral fat accumulation [120]. Notably, adipocyte-derived exosomes are essential for liver physiological activity [121].…”

Section: Obesitymentioning

confidence: 99%

The crosstalk: exosomes and lipid metabolism

et al. 2020

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Exosomes have been considered as novel and potent vehicles of intercellular communication, instead of "cell dust". Exosomes are consistent with anucleate cells, and organelles with lipid bilayer consisting of the proteins and abundant lipid, enhancing their "rigidity" and "flexibility". Neighboring cells or distant cells are capable of exchanging genetic or metabolic information via exosomes binding to recipient cell and releasing bioactive molecules, such as lipids, proteins, and nucleic acids. Of note, exosomes exert the remarkable effects on lipid metabolism, including the synthesis, transportation and degradation of the lipid. The disorder of lipid metabolism mediated by exosomes leads to the occurrence and progression of diseases, such as atherosclerosis, cancer, nonalcoholic fatty liver disease (NAFLD), obesity and Alzheimer's diseases and so on. More importantly, lipid metabolism can also affect the production and secretion of exosomes, as well as interactions with the recipient cells. Therefore, exosomes may be applied as effective targets for diagnosis and treatment of diseases.

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Section: Obesitymentioning

confidence: 99%

The crosstalk: exosomes and lipid metabolism

et al. 2020

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“…In addition, the plasma exosomal transcription release factor (PTRF) increases the occurrence of hypertrophy and aging of 3 T3-L1 adipocytes. Circulating polymerase I and PTRF, like adipokines, may partially contribute to the deleterious effects of visceral fat accumulation [90]. Notably, adipocyte-derived exosomes are essential for liver physiological activity [91].…”

Section: The Pathological Roles Of Mirnas In Obesity and Diabetes: Pancreatic Islets And Adipose Tissuementioning

confidence: 99%

Does microRNA Perturbation Control the Mechanisms Linking Obesity and Diabetes? Implications for Cardiovascular Risk

Sala

Crestani

Garavelli

et al. 2020

IJMS

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Metabolic disorders such as obesity and type 2 diabetes (T2D) are considered the major risk factors for the development of cardiovascular diseases (CVD). Although the pathological mechanisms underlying the mutual development of obesity and T2D are difficult to define, a better understanding of the molecular aspects is of utmost importance to identify novel therapeutic targets. Recently, a class of non-coding RNAs, called microRNAs (miRNAs), are emerging as key modulators of metabolic abnormalities. There is increasing evidence supporting the role of intra- and extracellular miRNAs as determinants of the crosstalk between adipose tissues, liver, skeletal muscle and other organs, triggering the paracrine communication among different tissues. miRNAs may be considered as risk factors for CVD due to their correlation with cardiovascular events, and in particular, may be related to the most prominent risk factors. In this review, we describe the associations observed between miRNAs expression levels and the most common cardiovascular risk factors. Furthermore, we sought to depict the molecular aspect of the interplay between obesity and diabetes, investigating the role of microRNAs in the interorgan crosstalk. Finally, we discussed the fascinating hypothesis of the loss of protective factors, such as antioxidant defense systems regulated by such miRNAs.

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“…Several studies have demonstrated that adipose tissue produces adipokines that regulate lipid storage via endocrine and paracrine signals ( Perez-Diaz et al, 2018 ; Hörbelt et al, 2019 ). For example, polymerase I and transcription release factor is secreted from adipocytes and it induces lipid accumulation in both hepatocytes and adipocytes ( Perez-Diaz et al, 2018 ). Recently, microRNAs (miRNAs) have emerged as novel endocrine and paracrine signals ( Peng & Wang, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

High fructose exposure modifies the amount of adipocyte-secreted microRNAs into extracellular vesicles in supernatants and plasma

Hernández-Díazcouder

González-Ramírez

Giacoman-Martínez

et al. 2021

PeerJ

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Background High fructose exposure induces metabolic and endocrine responses in adipose tissue. Recent evidence suggests that microRNAs in extracellular vesicles are endocrine signals secreted by adipocytes. Fructose exposure on the secretion of microRNA by tissues and cells is poorly studied. Thus, the aim of this study was to evaluate the effect of fructose exposure on the secretion of selected microRNAs in extracellular vesicles from 3T3-L1 cells and plasma from Wistar rats. Methods 3T3-L1 cells were exposed to 550 µM of fructose or standard media for four days, microRNAs levels were determined in extracellular vesicles of supernatants and cells by RT-qPCR. Wistar rats were exposed to either 20% fructose drink or tap water for eight weeks, microRNAs levels were determined in extracellular vesicles of plasma and adipose tissue by RT-qPCR. Results This study showed that fructose exposure increased the total number of extracellular vesicles released by 3T3-L1 cells (p = 0.0001). The levels of miR-143-5p were increased in extracellular vesicles of 3T3-L1 cells exposed to fructose (p = 0.0286), whereas miR-223-3p levels were reduced (p = 0.0286). Moreover, in plasma-derived extracellular vesicles, miR-143-5p was higher in fructose-fed rats (p = 0.001), whereas miR-223-3p (p = 0.022), miR-342-3p (p = 0.0011), miR-140-5p (p = 0.0129) and miR-146b-5p (p = 0.0245) were lower. Conclusion Fructose exposure modifies the levels of microRNAs in extracellular vesicles in vitro and in vivo. In particular, fructose exposure increases miR-143-5p, while decreases miR-223-3p and miR-342-3p.

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PTRF acts as an adipokine contributing to adipocyte dysfunctionality and ectopic lipid deposition

Cited by 13 publications

References 24 publications

The crosstalk: exosomes and lipid metabolism

The crosstalk: exosomes and lipid metabolism

Does microRNA Perturbation Control the Mechanisms Linking Obesity and Diabetes? Implications for Cardiovascular Risk

High fructose exposure modifies the amount of adipocyte-secreted microRNAs into extracellular vesicles in supernatants and plasma

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