The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Inflammation and endoplasmic reticulum stress in obesity and diabetes
Open accessAbstract
Obesity is associated with chronic low-grade inflammation. Inflammatory signals interfere with insulin action and disrupt metabolic homeostasis. The c-Jun N-terminal kinase (JNK) has been identified as a central mediator of insulin resistance. Recent studies showed that in obesity compromising endoplasmic reticulum (ER) function results in insulin resistance and type 2 diabetes that are dependent on JNK activation. In contrast, enhancing ER function in transgenic mice or by the use of chemical chaperones protects against diet-induced insulin resistance. Hence, ER stress and the related signaling networks present a critical mechanism underlying obesity-induced JNK activity, inflammatory response and insulin resistance.
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Citations
Cites
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IL-6 Improves Energy and Glucose Homeostasis in Obesity via Enhanced Central IL-6 trans-Signaling
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cJun NH2-terminal kinase 1 (JNK1): Roles in metabolic regulation of insulin resistance
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Pedersen, B. K. (2019) · Annual Review of Physiology · doi:10.1146/annurev-physiol-020518-114339 · Cited by 163
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Karimzadeh, L., Behrouz, V., Sohrab, G., Hedayati, M., & Emami, G. (2022) · Journal of Food Science · doi:10.1111/1750-3841.16365 · Cited by 28
RLIP76 protein knockdown attenuates obesity due to a high-fat diet
Singhal, S. S., Figarola, J., Singhal, J., Reddy, M. A., Liu, X., Berz, D., Natarajan, R., & Awasthi, S. (2013) · Journal of Biological Chemistry · doi:10.1074/jbc.m113.480194 · Cited by 26
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Metadata
- Authors
- Hotamisligil, G. S.
- Venue
- International Journal of Obesity
- Published
- 2008-12
- Volume
- 32
- Issue
- S7
- Pages
- S52-S54
- ISSN
- 0307-0565 (ISSN-L)
- 1476-5497
- OpenAlex
- W2029442790
- Cited by
- 285
- References
- 5
- FWCI
- 10.73
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
