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Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance
Published on: February 17, 2023
[Insulin resistance and inflammation in chronic kidney diseases]
Fitsum Guebre-Egziabher1, Emilie Kalbacher, Denis Fouque
1Département de Néphrologie, Hôpital Edouard-Herriot, Lyon. fitsum-guebre-egziabher@chu-lyon.fr
Abstract:
Insulin resistance (IR) and inflammation are now identified as common features in chronic kidney disease (CKD) patients. These metabolic abnormalities are both predictors of adverse cardiovascular (CV) outcome and are associated with worst nutritional status. Unequivocal experimental, epidemiological and clinical evidence produced during the past decade causally links inflammation to the development of metabolic syndrome or the complications that emerge from these pathologies particularly in the context of obesity or type II diabetes patients. These observations lead to the hypothesis of "meta-inflammation" : metabolically triggered inflammation, with a key role played by adipose tissue. In CKD patients, many other factors related with uremia can be causative but the abnormal cytokine and adipokine concentrations and the cluster of metabolic abnormalities push us to think like other metabolic diseases, that adipose tissue dysfunction may be among the pathways that induce inflammation and IR. Therapeutic approaches of traditional CV risk factors have been inconclusive or failed to improve the outcome of these patients. Further studies assessing the impact of renal failure on adipose tissue function and the pathways that are altered in this disease may allow to have therapeutic approaches targetting adipose tissue dysfunction or inflammation.
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