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Citations to this article

Deletion of Fas in adipocytes relieves adipose tissue inflammation and hepatic manifestations of obesity in mice
Stephan Wueest, … , Marc Y. Donath, Daniel Konrad
Stephan Wueest, … , Marc Y. Donath, Daniel Konrad
Published December 1, 2009
Citation Information: J Clin Invest. 2010;120(1):191-202. https://doi.org/10.1172/JCI38388.
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Research Article Metabolism Article has an altmetric score of 1

Deletion of Fas in adipocytes relieves adipose tissue inflammation and hepatic manifestations of obesity in mice

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Abstract

Adipose tissue inflammation is linked to the pathogenesis of insulin resistance. In addition to exerting death-promoting effects, the death receptor Fas (also known as CD95) can activate inflammatory pathways in several cell lines and tissues, although little is known about the metabolic consequence of Fas activation in adipose tissue. We therefore sought to investigate the contribution of Fas in adipocytes to obesity-associated metabolic dysregulation. Fas expression was markedly increased in the adipocytes of common genetic and diet-induced mouse models of obesity and insulin resistance, as well as in the adipose tissue of obese and type 2 diabetic patients. Mice with Fas deficiency either in all cells or specifically in adipocytes (the latter are referred to herein as AFasKO mice) were protected from deterioration of glucose homeostasis induced by high-fat diet (HFD). Adipocytes in AFasKO mice were more insulin sensitive than those in wild-type mice, and mRNA levels of proinflammatory factors were reduced in white adipose tissue. Moreover, AFasKO mice were protected against hepatic steatosis and were more insulin sensitive, both at the whole-body level and in the liver. Thus, Fas in adipocytes contributes to adipose tissue inflammation, hepatic steatosis, and insulin resistance induced by obesity and may constitute a potential therapeutic target for the treatment of insulin resistance and type 2 diabetes.

Authors

Stephan Wueest, Reto A. Rapold, Desiree M. Schumann, Julia M. Rytka, Anita Schildknecht, Ori Nov, Alexander V. Chervonsky, Assaf Rudich, Eugen J. Schoenle, Marc Y. Donath, Daniel Konrad

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Total citations by year

Year: 2025 2024 2023 2022 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 2010 2009 Total
Citations: 4 6 5 3 5 6 6 3 4 5 6 5 8 9 11 6 1 93
Citation information
This citation data is accumulated from CrossRef, which receives citation information from participating publishers, including this journal. Not all publishers participate in CrossRef, so this information is not comprehensive. Additionally, data may not reflect the most current citations to this article, and the data may differ from citation information available from other sources (for example, Google Scholar, Web of Science, and Scopus).

Citations to this article in year 2010 (6)

Title and authors Publication Year
The Portal Theory Supported by Venous Drainage–Selective Fat Transplantation
JM Rytka, S Wueest, EJ Schoenle, D Konrad
Diabetes 2010
Toll-like receptor 2-deficient mice are protected from insulin resistance and beta cell dysfunction induced by a high-fat diet
JA Ehses, DT Meier, S Wueest, J Rytka, S Boller, PY Wielinga, A Schraenen, K Lemaire, S Debray, L Lommel, JA Pospisilik, O Tschopp, SM Schultze, U Malipiero, H Esterbauer, H Ellingsgaard, S Rütti, FC Schuit, TA Lutz, M Böni-Schnetzler, D Konrad, MY Donath
Diabetologia 2010
Comprehensive Physiology
R Terjung
Comprehensive Physiology 2010
Animal models of nonalcoholic fatty liver disease
L Hebbard, J George
Nature Reviews Gastroenterology & Hepatology 2010
Evidence for activation of inflammatory lipoxygenase pathways in visceral adipose tissue of obese Zucker rats
SK Chakrabarti, Y Wen, AD Dobrian, BK Cole, Q Ma, H Pei, MD Williams, MH Bevard, GE Vandenhoff, SR Keller, J Gu, JL Nadler
American journal of physiology. Endocrinology and metabolism 2010
The Role of Adipose Tissue and Lipotoxicity in the Pathogenesis of Type 2 Diabetes
K Cusi
Current Diabetes Reports 2010

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