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Inflammatory Process in Type 2 Diabetes: The Role of Cytokines
Abstract
Abstract: Population‐based studies have shown strong relationship between inflammatory markers and metabolic disturbances, obesity, and atherosclerosis, whereas inflammation has been considered as a “common soil” between these clinical entities and type 2 diabetes (T2D). The accumulation of macrophages in adipose tissue (AT), the common origin of macrophages and adipocytes, the prevalent presence of peripheral mononuclear cells, and apoptotic β cells by themselves seem to be the sources of inflammation present in T2D, since they generate the mediators of the inflammatory processes, namely cytokines. The main cytokines involved in the pathogenesis of T2D are interleukin‐1β (IL‐1β), with an action similar to the one present in type 1 diabetes, tumor necrosis factor‐α (TNF‐α), and IL‐6, considered as the main regulators of inflammation, leptin, more recently introduced, and several others, such as monocyte chemoattractant protein‐1, resistin, adiponectin, with either deleterious or beneficial effects in diabetic pathogenesis. The characterization of these molecules targeted diabetes treatment beyond the classical interventions with lifestyle changes and pharmaceutical agents, and toward the determination of specific molecular pathways that lead to low grade chronic inflammatory state mainly due to an immune system's unbalance.
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“Type 2 diabetes, obesity, and cardiovascular disease are related to a state of low-grade systemic inflammation [7, 27–29].”
From Exercise as a Mean to Control Low‐Grade Systemic Inflammation (2008) · cites this paper as [29]
In the citing paper
“Thus, a number of studies indicate that elevated TNF-α is not secondary to the pathological conditions associated with insulin resistance, but that TNF-α plays a direct pathogenic role in glucose metabolism [29, 40].”
From Exercise as a Mean to Control Low‐Grade Systemic Inflammation (2008) · cites this paper as [29]
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Metadata
- Authors
- ALEXANDRAKI, K., PIPERI, C., KALOFOUTIS, C., SINGH, J., ALAVERAS, A., & KALOFOUTIS, A.
- Affiliations
- National and Kapodistrian University of Athens (GR)
- University of Lancashire (GB)
- Corresponding author
- PIPERI, CHRISTINA
- Venue
- Annals of the New York Academy of Sciences
- Publisher
- Wiley
- Published
- 2006-11
- Volume
- 1084
- Issue
- 1
- Pages
- 89-117
- ISSN
- 0077-8923 (ISSN-L)
- 1749-6632
- OpenAlex
- W1491280754
- Semantic Scholar
- 160271b5b2f5d455bde3b3b6558683292a30fa1c
- Cited by
- 309
- References
- 281
- Citations by year
- 2026: 7 · 2025: 9 · 2024: 21 · 2023: 13 · 2022: 11 · 2021: 16 · 2020: 12 · 2019: 11 · 2018: 19 · 2017: 15 · 2016: 17 · 2015: 14 · 2014: 22 · 2013: 20 · 2012: 14
- FWCI
- 2.18
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annals of the New York Academy of Sciences (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Keywords
- type 2 diabetes, inflammation, adipose tissue macrophages, cytokines, IL-1β, TNF-α, interleukin-6, leptin, adiponectin, resistin, MCP-1, beta-cell apoptosis, obesity, atherosclerosis, low-grade inflammation, immune dysregulation
- MeSH terms
- Animals, Diabetes Mellitus, Experimental, Diabetes Mellitus, Type 2, Humans, Inflammation, Cytokines
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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