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Inflammation and insulin resistance
Open accessAbstract
Obesity‐induced chronic inflammation is a key component in the pathogenesis of insulin resistance and the Metabolic syndrome. In this review, we focus on the interconnection between obesity, inflammation and insulin resistance. Pro‐inflammatory cytokines can cause insulin resistance in adipose tissue, skeletal muscle and liver by inhibiting insulin signal transduction. The sources of cytokines in insulin resistant states are the insulin target tissue themselves, primarily fat and liver, but to a larger extent the activated tissue resident macrophages. While the initiating factors of this inflammatory response remain to be fully determined, chronic inflammation in these tissues could cause localized insulin resistance via autocrine/paracrine cytokine signaling and systemic insulin resistance via endocrine cytokine signaling all of which contribute to the abnormal metabolic state.
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In the citing paper
“Evidence indicates that inflammation causes insulin resistance”
From Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty (2018) · cites this paper as [281]
In the citing paper
“The intake of flavonols and flavones was not correlated with plasma concentrations of CRP or IL-6 in healthy women (BMI 25•8-26•2 kg/m 2 ) (801) .”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [801]
In the citing paper
“Several cytokines and chemokines, such as CCL2, IL-6, IL-1β, macrophage migration inhibitory factor (MIF), and TNF-α, can be released by adipocytes and macrophages (83)(84)(85).”
From Insulin sensitivity: Modulation by nutrients and inflammation (2008) · cites this paper as [83]
In the citing paper
“Adipocytes are the unique source of secreted adipokines such as leptin and adiponectin, which can promote insulin sensitivity, as well as resistin and retinol-binding protein 4 (RBP4), which can impair insulin sensitivity (83)(84)(85).”
From Insulin sensitivity: Modulation by nutrients and inflammation (2008) · cites this paper as [83]
In the citing paper
“Consistent with this, elevated levels of the proinflammatory cytokines TNF-α, IL-6, and C-reactive protein (CRP) have been shown in individuals with insulin resistance and diabetes (for review, see refs.[83][84][85].”
From Insulin sensitivity: Modulation by nutrients and inflammation (2008) · cites this paper as [83]
In the citing paper
“NO suppresses the TLR4-mediated inflammation and ROS production by inactivating IkB kinase-β/nuclear factor-κB (IκκB/NF-κβ) [9,63]”
From NO-Rich Diet for Lifestyle-Related Diseases (2015) · cites this paper as [63]
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Metadata
- Authors
- de Luca, C., & Olefsky, J. M.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- Olefsky, Jerrold M.
- ORCID
- Olefsky, Jerrold M.
- Venue
- FEBS Letters
- Publisher
- Wiley
- Published
- 2007-11-29
- Volume
- 582
- Issue
- 1
- Pages
- 97-105
- ISSN
- 0014-5793 (ISSN-L)
- 1873-3468
- PMC
- PMC2246086
- OpenAlex
- W2031882974
- Cited by
- 1,161
- References
- 66
- Citations by year
- 2026: 56 · 2025: 68 · 2024: 54 · 2023: 83 · 2022: 82 · 2021: 83 · 2020: 68 · 2019: 64 · 2018: 73 · 2017: 69 · 2016: 58 · 2015: 56 · 2014: 40 · 2013: 65 · 2012: 58
- FWCI
- 5.45
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- FEBS Letters (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 074868, DK 033651, T32DK007494, R37DK033651, DK007494, P01DK074868)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (U54HD012303)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- insulin resistance, obesity, chronic inflammation, metabolic syndrome, inflammatory cytokines, adipose tissue, skeletal muscle, liver, insulin signaling, macrophages, autocrine and paracrine signaling
- MeSH terms
- Humans, Inflammation, Insulin Resistance, Signal Transduction
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