Inflammation and insulin resistance
Open accessAbstract
Over a hundred years ago, high doses of salicylates were shown to lower glucose levels in diabetic patients. This should have been an important clue to link inflammation to the pathogenesis of type 2 diabetes (T2D), but the antihyperglycemic and antiinflammatory effects of salicylates were not connected to the pathogenesis of insulin resistance until recently. Together with the discovery of an important role for tissue macrophages, these new findings are helping to reshape thinking about how obesity increases the risk for developing T2D and the metabolic syndrome. The evolving concept of insulin resistance and T2D as having immunological components and an improving picture of how inflammation modulates metabolism provide new opportunities for using antiinflammatory strategies to correct the metabolic consequences of excess adiposity.
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Inflammatory signals such as tumour necrosis factor α and interleukin 6 activate serine and threonine kinases such as Iκ kinase β and jun-N terminal kinase, which have been implicated in increased serine phosphorylation of IRS1.
“Specifically, inflammatory signals such as tumour necrosis factor α and interleukin 6 activate serine and threonine kinases such as Iκ kinase β and jun-N terminal kinase, which have been implicated in increased serine phosphor ylation of IRS1.”
From Lipid-induced insulin resistance: unravelling the mechanism (2010) · cites this paper as [117]
Inflammatory signals affect cellular pathways that intersect with insulin action.
“Mechanistically, inflammatory signals affect cellular pathways that intersect with insulin action.117”
From Lipid-induced insulin resistance: unravelling the mechanism (2010) · cites this paper as [117]
Elevated levels of IL-1β are observed in pancreatic islet cells from patients with type 2 diabetes, which is increasingly being recognized as having a strong inflammatory component.
“elevated levels of IL-1β are also observed in the pancreatic islet cells from patients with type 2 diabetes46, which is increasingly being recognized as having a strong inflammatory component47.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [47]
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- Authors
- Shoelson, S. E.
- Affiliations
- Joslin Diabetes Center (US)
- Corresponding author
- Shoelson, S. E.
- ORCID
- Shoelson, S. E.
- Venue
- Journal of Clinical Investigation
- Published
- 2006-07-03
- Volume
- 116
- Issue
- 7
- Pages
- 1793-1801
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC1483173
- OpenAlex
- W2152377123
- Cited by
- 4,769
- References
- 106
- Citations by year
- 2026: 210 · 2025: 222 · 2024: 207 · 2023: 216 · 2022: 231 · 2021: 224 · 2020: 225 · 2019: 226 · 2018: 228 · 2017: 251 · 2016: 274 · 2015: 284 · 2014: 315 · 2013: 345 · 2012: 323
- FWCI
- 20.08
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- inflammation, insulin resistance, type 2 diabetes, salicylates, anti-inflammatory therapy, tissue macrophages, obesity, metabolic syndrome, adiposity
- MeSH terms
- Anti-Inflammatory Agents, Clinical Trials as Topic, Diabetes Mellitus, Type 2, Humans, Inflammation, Insulin Resistance, Liver, Obesity, Signal Transduction, Adipocytes
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