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Cells
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Adipose Tissue, Obesity, and Metabolic Diseases
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Adipose Tissue, Obesity, and Metabolic Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Metabolism".

Deadline for manuscript submissions: 31 March 2025 | Viewed by 1727

Special Issue Editor

Dr. Takafumi Miyamoto

E-Mail Website
Guest Editor
Department of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, University of Tsukuba, Tsukuba 305-8577, Japan
Interests: planetary health nutrition; synthetic biology; signaling dynamics; organelle morphology

Special Issue Information

Dear Colleagues,

Struggles against hunger represent a significant aspect of human history, but recent technological innovations are promising to end this. However, the widespread availability of high-fat diets due to advancements in animal husbandry and food processing has increased obesity and metabolic diseases, posing urgent global health challenges. Research in molecular biology, genetics, optics, and bioinformatics has shown that adipose tissue is not just a fat storage depot but plays a crucial role in energy balance, endocrine function, and lipotoxicity. These findings have highlighted the complex pathways governing adipose tissue dynamics and their relationships with multiple organs, impacting metabolic diseases. Despite these advances, much still remains to be discovered.

This Special Issue, “Adipose Tissue, Obesity, and Metabolic Diseases”, will collect relevant research to allow a deep understanding of the role of adipose tissue role in metabolic diseases, aiming to pave the way for innovative therapeutic strategies to combat obesity and its complications.

Dr. Takafumi Miyamoto
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • adipose tissue
  • obesity
  • metabolic diseases
  • stress
  • inflammation
  • gut microbiota

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Published Papers (2 papers)

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Research

17 pages, 3925 KiB  
Article
Adipose Tissue Macrophages of the Human Fetus
by Ádám Radványi, Katalin Gyurina, Emese Rácz, Ilona Kovács, Gábor Méhes and Tamás Röszer
Cells 2024, 13(21), 1787; https://doi.org/10.3390/cells13211787 - 28 Oct 2024
Viewed by 503
Abstract
Prenatal adipose tissue development affects body composition and growth trajectory in early infancy, therefore it is a key determinant of adiposity in childhood. Childhood overweight and obesity increase the probability of being obese as an adult. After birth and in adulthood, adipose tissue [...] Read more.
Prenatal adipose tissue development affects body composition and growth trajectory in early infancy, therefore it is a key determinant of adiposity in childhood. Childhood overweight and obesity increase the probability of being obese as an adult. After birth and in adulthood, adipose tissue macrophages (ATMs) are relevant constituents of the fat depots, and they are necessary for physiological adipose tissue development and fat metabolism. In obesity, however, ATMs may induce chronic inflammation leading to insulin resistance, pancreatic beta cell damage and self-immunity. Despite being relevant regulators of adipose tissue development and functioning, it is unknown whether ATMs are present in the fetal adipose tissue, therefore it is elusive whether they may affect the prenatal establishment of fat depots. Here we studied the distribution of ATMs in the human fetus between gestational weeks 17 and 38 and labeled ATMs in the early postnatal life. We found that CD45+/CD14+/CD68+ ATMs infiltrated the fetal adipose tissue from the 17th week of gestation and remained persistent throughout the second and third trimesters. ATMs were phagocytic in the neonate and expressed interleukin-6, along with other pro-inflammatory gene products. These findings show that ATMs colonize the adipose tissue early in gestation, raising the possibility that intrauterine ATM–adipocyte communication may exist, eventually allowing ATMs to affect prenatal adipose tissue development. Full article
(This article belongs to the Special Issue Adipose Tissue, Obesity, and Metabolic Diseases)
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16 pages, 5929 KiB  
Article
Neddylation and Its Target Cullin 3 Are Essential for Adipocyte Differentiation
by Hongyi Zhou, Vijay Patel, Robert Rice, Richard Lee, Ha Won Kim, Neal L. Weintraub, Huabo Su and Weiqin Chen
Cells 2024, 13(19), 1654; https://doi.org/10.3390/cells13191654 - 5 Oct 2024
Viewed by 980
Abstract
The ongoing obesity epidemic has raised awareness of the complex physiology of adipose tissue. Abnormal adipocyte differentiation results in the development of systemic metabolic disorders such as insulin resistance and diabetes. The conjugation of NEDD8 (neural precursor cell expressed, developmentally downregulated 8) to [...] Read more.
The ongoing obesity epidemic has raised awareness of the complex physiology of adipose tissue. Abnormal adipocyte differentiation results in the development of systemic metabolic disorders such as insulin resistance and diabetes. The conjugation of NEDD8 (neural precursor cell expressed, developmentally downregulated 8) to target protein, termed neddylation, has been shown to mediate adipogenesis. However, much remains unknown about its role in adipogenesis. Here, we demonstrated that neddylation and its targets, the cullin (CUL) family members, are differentially regulated during mouse and human adipogenesis. Inhibition of neddylation by MLN4924 significantly reduced adipogenesis of 3T3-L1 and human stromal vascular cells. Deletion of NAE1, a subunit of the only NEDD8 E1 enzyme, suppressed neddylation and impaired adipogenesis. Neddylation deficiency did not affect mitotic cell expansion. Instead, it disrupted CREB/CEBPβ/PPARγ signaling, essential for adipogenesis. Interestingly, among the neddylation-targeted CUL family members, deletion of CUL3, but not CUL1, CUL2, or CUL4A, largely replicated the adipogenic defects observed with neddylation deficiency. A PPARγ agonist minimally rescued the adipogenic defects caused by the deletion of NAE1 and CUL3. In conclusion, our study demonstrates that neddylation and its targeted CUL3 are crucial for adipogenesis. These findings provide potential targets for therapeutic intervention in obesity and metabolic disorders. Full article
(This article belongs to the Special Issue Adipose Tissue, Obesity, and Metabolic Diseases)
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