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Inter-organ cross-talk in metabolic syndrome
Abstract
Maintenance of systemic homeostasis and the response to nutritional and environmental challenges require the coordination of multiple organs and tissues. To respond to various metabolic demands, higher organisms have developed a system of inter-organ communication through which one tissue can affect metabolic pathways in a distant tissue. Dysregulation of these lines of communication contributes to human pathologies, including obesity, diabetes, liver disease and atherosclerosis. In recent years, technical advances such as data-driven bioinformatics, proteomics and lipidomics have enabled efforts to understand the complexity of systemic metabolic cross-talk and its underlying mechanisms. Here, we provide an overview of inter-organ signals and their roles in metabolic control, and highlight recent discoveries in the field. We review peptide, small-molecule and lipid mediators secreted by metabolic tissues, as well as the role of the central nervous system in orchestrating peripheral metabolic functions. Finally, we discuss the contributions of inter-organ signalling networks to the features of metabolic syndrome.
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“To our knowledge, no review has provided a comprehensive integrative overview of these novel molecular players and the mechanisms involved in the redistribution of metabolic fuel during and after exercise, the loss of weight and fat mass, and reduced inflammation.”
In the citing paper
“Literature on this topic is vast and has been reviewed by others but on a separate basis, by describing either individual molecules or groups of factors, proteins, hormones, or molecules [2,3,4,5,6,7,8,9,29].”
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“could thus be at least partially responsible for preventing, or even reverting, obesity and the obesity-associated metabolic dysfunction in target organs”
In the citing paper
“novel circulating molecules induced by exercise, such as myokines, hepatokines, osteokines, immune cytokines, and adipokines regulate metabolic pathways and inter-tissue crosstalk by means of autocrine, paracrine, and endocrine effects [2]”
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Metadata
- Authors
- Priest, C., & Tontonoz, P.
- Affiliations
- University of California, Los Angeles (US)
- Corresponding author
- Tontonoz, Peter
- ORCID
- Tontonoz, Peter
- Venue
- Nature Metabolism
- Published
- 2019-12-09
- Volume
- 1
- Issue
- 12
- Pages
- 1177-1188
- ISSN
- 2522-5812 (ISSN-L)
- OpenAlex
- W2993039085
- Cited by
- 279
- References
- 209
- Citations by year
- 2026: 36 · 2025: 47 · 2024: 54 · 2023: 50 · 2022: 46 · 2021: 27 · 2020: 19
- FWCI
- 3.39
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Nature Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK120851)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Keywords
- inter-organ communication, metabolic syndrome, systemic homeostasis, obesity, diabetes mellitus, liver disease, atherosclerosis, lipid mediators, central nervous system regulation
- MeSH terms
- Animals, Energy Metabolism, Homeostasis, Humans, Receptor Cross-Talk, Metabolic Syndrome
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