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Contribution of Adipose Tissue Inflammation to the Development of Type 2 Diabetes Mellitus
Open accessAbstract
The objective of this comprehensive review is to summarize and discuss the available evidence of how adipose tissue inflammation affects insulin sensitivity and glucose tolerance. Low‐grade, chronic adipose tissue inflammation is characterized by infiltration of macrophages and other immune cell populations into adipose tissue, and a shift toward more proinflammatory subtypes of leukocytes. The infiltration of proinflammatory cells in adipose tissue is associated with an increased production of key chemokines such as C‐C motif chemokine ligand 2, proinflammatory cytokines including tumor necrosis factor α and interleukins 1β and 6 as well as reduced expression of the key insulin‐sensitizing adipokine, adiponectin. In both rodent models and humans, adipose tissue inflammation is consistently associated with excess fat mass and insulin resistance. In humans, associations with insulin resistance are stronger and more consistent for inflammation in visceral as opposed to subcutaneous fat. Further, genetic alterations in mouse models of obesity that reduce adipose tissue inflammation are—almost without exception—associated with improved insulin sensitivity. However, a dissociation between adipose tissue inflammation and insulin resistance can be observed in very few rodent models of obesity as well as in humans following bariatric surgery‐ or low‐calorie‐diet‐induced weight loss, illustrating that the etiology of insulin resistance is multifactorial. Taken together, adipose tissue inflammation is a key factor in the development of insulin resistance and type 2 diabetes in obesity, along with other factors that likely include inflammation and fat accumulation in other metabolically active tissues. © 2019 American Physiological Society.Compr Physiol 9:1‐58, 2019.
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A Stress Signaling Pathway in Adipose Tissue Regulates Hepatic Insulin Resistance
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Chronic Adipose Tissue Inflammation Linking Obesity to Insulin Resistance and Type 2 Diabetes
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Chronic Low Grade Inflammation in Pathogenesis of PCOS
Rudnicka, E., Suchta, K., Grymowicz, M., Calik-Ksepka, A., Smolarczyk, K., Duszewska, A. M., Smolarczyk, R., & Meczekalski, B. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22073789 · Cited by 680
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Saponaro, C., Sabatini, S., Gaggini, M., Carli, F., Rosso, C., Positano, V., Armandi, A., Caviglia, G. P., Faletti, R., Bugianesi, E., et al. (2022) · Liver International · doi:10.1111/liv.15377 · Cited by 116
Metadata
- Authors
- Burhans, M. S., Hagman, D. K., Kuzma, J. N., Schmidt, K. A., & Kratz, M.
- Venue
- Comprehensive Physiology
- Publisher
- Wiley
- Published
- 2018-12-13
- Volume
- 9
- Issue
- 1
- Pages
- 1-58
- ISSN
- 2040-4603 (ISSN-L)
- OpenAlex
- W2905533535
- Cited by
- 373
- References
- 570
- Type
- other
- Language
- en
- Open access
- green
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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Data sources
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.