Integrative systems analysis of diet-induced obesity identified a critical transition in the transcriptomes of the murine liver and epididymal white adipose tissue

Kim, Jeewon; Ey, Kwon; Park, S; Kim, J-R; Choi, Sw; Choi, Man‐Yeon; Sj, Kim

doi:10.1038/ijo.2015.147

Cited by 7 publications

(5 citation statements)

References 50 publications

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“…Although the RefSeq data show that Ic and Id include alternative start codons that produce alternative protein isoforms, the functional significance of either isoform has not yet been validated. MafF is induced by proinflammatory cytokines in myometrial cells (Massrieh et al, 2006), and it is upregulated in the livers of diet-induced obesity mouse models (Kim et al, 2015). …”

Section: Gene Structure and Expression Profile Of Smafsmentioning

confidence: 99%

Small Maf proteins (MafF, MafG, MafK): History, structure and function

Katsuoka

Yamamoto

2016

Gene

204

152

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The small Maf proteins (sMafs) are basic region leucine zipper (bZIP)-type transcription factors. The basic region of the Maf family is unique among the bZIP factors, and it contributes to the distinct DNA-binding mode of this class of proteins. MafF, MafG and MafK are the three vertebrate sMafs, and no functional differences have been observed among them in terms of their bZIP structures. sMafs form homodimers by themselves, and they form heterodimers with cap ‘n’ collar (CNC) proteins (p45 NF-E2, Nrf1, Nrf2, and Nrf3) and also with Bach proteins (Bach1 and Bach2). Because CNC and Bach proteins cannot bind to DNA as monomers, sMafs are indispensable partners that are required by CNC and Bach proteins to exert their functions. sMafs lack the transcriptional activation domain; hence, their homodimers act as transcriptional repressors. In contrast, sMafs participate in transcriptional activation or repression depending on their heterodimeric partner molecules and context. Mouse genetic analyses have revealed that various biological pathways are under the regulation of CNC-sMaf heterodimers. In this review, we summarize the history and current progress of sMaf studies in relation to their partners.

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Section: Gene Structure and Expression Profile Of Smafsmentioning

confidence: 99%

Small Maf proteins (MafF, MafG, MafK): History, structure and function

Katsuoka

Yamamoto

2016

Gene

204

152

View full text Add to dashboard Cite

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“…76 On the basis of some reports, eWAT has been considered as a target site for this regulatory cricuit. [77][78][79][80][81] Finally, the whole circadian variation of gut microbiota has not been focused on. Considering the strong associations between these symbionts and host, the hypothesis has been proposed whether significant metabolic changes would be triggered by the overlap or stagger of both, namely whether rhythmic disorder-induced alternation of gut microbiota contributed to shaping host physiology.…”

Section: Discussionmentioning

confidence: 99%

The Mechanism of Oral Melatonin Ameliorates Intestinal and Adipose Lipid Dysmetabolism Through Reducing Escherichia Coli-Derived Lipopolysaccharide

Rong

Reíter

et al. 2021

Cellular and Molecular Gastroenterology and Hepatology

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“…Based on some references, we considered epididymal WAT as an important tissue for metabolic syndrome and primarily measured its physiological changes in this investigation. [79][80][81][82][83] Finally, dosage of melatonin injection in our experiment was conducted in strict accordance with pharmacological guidance standards. However, we and others did not detect viability of adipocytes to be affected under this dose, while melatonin regulated multiple physiological functions in adipocytes.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, epididymal WAT is tightly wrapped by mature vessels, indicating that it may be more beneficial to extra transportation of adipose‐derived products. Based on some references, we considered epididymal WAT as an important tissue for metabolic syndrome and primarily measured its physiological changes in this investigation . Finally, dosage of melatonin injection in our experiment was conducted in strict accordance with pharmacological guidance standards.…”

Section: Discussionmentioning

confidence: 99%

Reduced delivery of epididymal adipocyte‐derived exosomal resistin is essential for melatonin ameliorating hepatic steatosis in mice

Rong

Feng

Liu

et al. 2019

Journal of Pineal Research

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Adipocyte‐derived exosomes (Exos) serve as bioinformation‐containing messengers in cell‐to‐cell communications, and numerous reports demonstrate that resistin, an adipokine, is strongly associated with hepatic steatosis and other fatty liver diseases, suggesting that adipose dysfunction‐generated altered pattern of exosomal cytokines may contribute to shaping the physiological activities in liver. Admittedly, melatonin‐mediated positive effects on various tissues/organs have been respectively reported, but regulatory mechanisms of melatonin on the crosstalk between adipose tissue and liver have been investigated rarely. Overall, we hypothesize that the crosstalk originating from adipose tissue may be another worthy regulatory pathway for melatonin ameliorating of hepatic steatosis. Here, we first found the amount of adipocyte‐derived exosomal resistin to be significantly decreased by melatonin supplementation. Compared to mice with ExosHFD or Exosresistin treatment, ExosMT remarkably ameliorated hepatic steatosis. Further test demonstrated that resistin was a pivotal cytokine which repressed phosphorylation of 5′ adenosine monophosphate‐activated protein kinase α (pAMPKα Thr172) to trigger endoplasmic reticulum (ER) stress, resulting in hepatic steatosis, whereas ExosMT reversed these risks in hepatocytes. In adipocytes, we identified melatonin to reduce the production of resistin through the brain and muscle arnt‐like protein 1 (Bmal1) transcriptional inhibition. Notably, we also confirmed that melatonin enhanced N6‐Methyladenosine (m6A) RNA demethylation to degrade resistin mRNA in adipocytes. Overall, melatonin decreases traffic volume of adipocyte‐generated exosomal resistin from adipocytes to hepatocytes, which further alleviates ER stress‐induced hepatic steatosis. Our findings illustrate a novel melatonin‐mediated regulatory pathway from adipocytes to hepatocytes, indicating that adipocyte‐derived exosome is a new potential target for treating obesity and related hepatorenal syndrome.

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Integrative systems analysis of diet-induced obesity identified a critical transition in the transcriptomes of the murine liver and epididymal white adipose tissue

Abstract: In this study, systems analysis identified regulatory network modules underlying the delayed immune system-related pathological changes during the development of DIO and could suggest possible therapeutic targets.

Cited by 7 publications

References 50 publications

Small Maf proteins (MafF, MafG, MafK): History, structure and function

Small Maf proteins (MafF, MafG, MafK): History, structure and function

The Mechanism of Oral Melatonin Ameliorates Intestinal and Adipose Lipid Dysmetabolism Through Reducing Escherichia Coli-Derived Lipopolysaccharide

Reduced delivery of epididymal adipocyte‐derived exosomal resistin is essential for melatonin ameliorating hepatic steatosis in mice

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