The DOI matches its Crossref record; 78 of the 78 references it cites were found in a registry or an index.
β Cell dysfunction during progression of metabolic syndrome to type 2 diabetes
Open accessAbstract
In a society where physical activity is limited and food supply is abundant, metabolic diseases are becoming a serious epidemic. Metabolic syndrome (MetS) represents a cluster of metabolically related symptoms such as obesity, hypertension, dyslipidemia, and carbohydrate intolerance, and significantly increases type 2 diabetes mellitus risk. Insulin resistance and hyperinsulinemia are consistent characteristics of MetS, but which of these features is the initiating insult is still widely debated. Regardless, both of these conditions trigger adverse responses from the pancreatic β cell, which is responsible for producing, storing, and releasing insulin to maintain glucose homeostasis. The observation that the degree of β cell dysfunction correlates with the severity of MetS highlights the need to better understand β cell dysfunction in the development of MetS. This Review focuses on the current understanding from rodent and human studies of the progression of β cell responses during the development of MetS, as well as recent findings addressing the complexity of β cell identity and heterogeneity within the islet during disease progression. The differential responses observed in β cells together with the heterogeneity in disease phenotypes within the patient population emphasize the need to better understand the mechanisms behind β cell adaptation, identity, and dysfunction in MetS.
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Cites
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Cited by
Obesity and type 2 diabetes mellitus: connections in epidemiology, pathogenesis, and treatments
Ruze, R., Liu, T., Zou, X., Song, J., Chen, Y., Xu, R., Yin, X., & Xu, Q. (2023) · Frontiers in Endocrinology · doi:10.3389/fendo.2023.1161521 · Cited by 799
The Role of Oxidative Stress in Pancreatic β Cell Dysfunction in Diabetes
Eguchi, N., Vaziri, N. D., Dafoe, D. C., & Ichii, H. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22041509 · Cited by 341
Yaribeygi, H., Maleki, M., Sathyapalan, T., Jamialahmadi, T., & Sahebkar, A. (2021) · Journal of Diabetes Research · doi:10.1155/2021/7796727 · Cited by 91
Metabolic syndrome and its association with nonalcoholic steatohepatitis
Bril, F., Sanyal, A., & Cusi, K. (2023) · Clinics in Liver Disease · doi:10.1016/j.cld.2023.01.002 · Cited by 52
Corezola do Amaral, M. E., Kravets, V., Dwulet, J. M., Farnsworth, N. L., Piscopio, R., Schleicher, W. E., Miranda, J. G., & Benninger, R. K. P. (2020) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00132.2020 · Cited by 41
Metadata
- Authors
- Hudish, L. I., Reusch, J. E. B., & Sussel, L.
- Venue
- Journal of Clinical Investigation
- Published
- 2019-08-19
- Volume
- 129
- Issue
- 10
- Pages
- 4001-4008
- ISSN
- 0021-9738 (ISSN-L)
- 1558-8238
- OpenAlex
- W2968775432
- Cited by
- 336
- References
- 78
- FWCI
- 28.52
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Hudish, L. I., Reusch, J. E. B., & Sussel, L. (2019). β Cell dysfunction during progression of metabolic syndrome to type 2 diabetes. Journal of Clinical Investigation. https://doi.org/10.1172/jci129188
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
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.