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 612

Special Issue Editor


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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

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Keywords

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

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Published Papers (1 paper)

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Research

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
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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