Adiponectin signaling and function in insulin target tissues
Open accessAbstract
Obesity-linked type 2 diabetes is one of the paramount causes of morbidity and mortality worldwide, posing a major threat on human health, productivity, and quality of life. Despite great progress made towards a better understanding of the molecular basis of diabetes, the available clinical counter-measures against insulin resistance, a defect that is central to obesity-linked type 2 diabetes, remain inadequate. Adiponectin, an abundant adipocyte-secreted factor with a wide-range of biological activities, improves insulin sensitivity in major insulin target tissues, modulates inflammatory responses, and plays a crucial role in the regulation of energy metabolism. However, adiponectin as a promising therapeutic approach has not been thoroughly explored in the context of pharmacological intervention, and extensive efforts are being devoted to gain mechanistic understanding of adiponectin signaling and its regulation, and reveal therapeutic targets. Here, we discuss tissue- and cell-specific functions of adiponectin, with an emphasis on the regulation of adiponectin signaling pathways, and the potential crosstalk between the adiponectin and other signaling pathways involved in metabolic regulation. Understanding better just why and how adiponectin and its downstream effector molecules work will be essential, together with empirical trials, to guide us to therapies that target the root cause(s) of type 2 diabetes and insulin resistance.
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Interaction between APPL1 and Rab5 may also contribute to GLUT4 translocation.
“Alternatively, interaction between APPL1 and Rab5 (a small GTPase) may also contribute.”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [55]
This translocation results from stimulating p38 MAPK via either AMPK or interaction with APPL1.
“This translocation results from stimulating p38 MAPK via either AMPK [10,44] or interaction with APPL1 [55].”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [55]
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Chait, A., & den Hartigh, L. J. (2020) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2020.00022 · Cited by 1,529 · see citing works
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Adiponectin signaling and its role in bone metabolism
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- Authors
- Ruan, H., & Dong, L. Q.
- Affiliations
- The University of Texas at San Antonio Health Science Center (US)
- Corresponding author
- Ruan, Hong
- Dong, Lily Q.
- ORCID
- Dong, Lily Q.
- Venue
- Journal of Molecular Cell Biology
- Publisher
- Oxford University Press (OUP)
- Published
- 2016-03-18
- Volume
- 8
- Issue
- 2
- Pages
- 101-109
- ISSN
- 1674-2788 (ISSN-L)
- 1759-4685
- PMC
- PMC4816150
- OpenAlex
- W2304535577
- Cited by
- 395
- References
- 115
- Citations by year
- 2026: 20 · 2025: 26 · 2024: 36 · 2023: 27 · 2022: 33 · 2021: 50 · 2020: 56 · 2019: 41 · 2018: 39 · 2017: 46 · 2016: 18 · 2015: 1
- FWCI
- 6.50
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Molecular Cell Biology (publishedVersion)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HighWire Press Open Archive (submittedVersion)
- Funders
- National Institutes of Health (R01 DK102965)
- American Diabetes Association (#7-13-BS-043)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- adiponectin, adiponectin signaling, type 2 diabetes, insulin resistance, insulin target tissues, obesity, energy metabolism, inflammation, metabolic crosstalk, therapeutic target
- MeSH terms
- Animals, Humans, Insulin, Models, Biological, Organ Specificity, Signal Transduction, Adiponectin, Receptors, Adiponectin
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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