Abstract
Nuclear erythroid factor 2 like 2 (Nrf2) has been described as a transcription factor that serves as a master regulator of the adaptive response to exogenous and endogenous oxidative and electrophilic stresses. Evidence of Nrf2 crosstalk with other molecular pathways is increasing; recent publications have proposed a role of Nrf2 in the development of obesity and in the highly regulated process of adipocyte differentiation through its interaction with other transcription factors and receptors implicated in metabolic regulation. In the present review, we discuss the available data on the possible role of Nrf2 in obesity and metabolic syndrome and the feasibility of using Nrf2 as a therapeutic target in the clinical setting.
Highlights
The present review aims to highlight the recent research progress that has been made in the field of the transcription factor Nuclear erythroid factor 2 like 2 (Nrf2) with reference to its role in the development of type 2 diabetes, obesity and metabolic syndrome and its potential use as a therapeutic target. the beneficial effects of a lifestyle change, in people who are already overweight or obese have become widely known [1, 2], the prevalence of obesity, metabolic syndrome and type 2 diabetes (T2D) continue to be high according to the US Center for Disease Control and Prevention
The present review aims to highlight the recent research progress that has been made in the field of the transcription factor Nrf2 with reference to its role in the development of type 2 diabetes, obesity and metabolic syndrome and its potential use as a therapeutic target
This study focused on white adipose tissue (WAT) and described that Nrf2 knock-out mice (Nrf2-KO) mice have lower amounts of WAT and the white adipocytes are smaller than in WT mice
Summary
The present review aims to highlight the recent research progress that has been made in the field of the transcription factor Nrf (nuclear erythroid factor 2 like 2) with reference to its role in the development of type 2 diabetes, obesity and metabolic syndrome and its potential use as a therapeutic target. MRNA levels of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1), a gluconeogenesis, fatty acid oxidation and mitochondrial biogenesis coordinator [47], and phosphoenolpyruvate carboxykinase (PEPCK),a key gluconeogenic enzyme, which are FGF21-regulated genes, were found to be increased in liver and WAT of Nrf2-KO mice These data suggest that the Nrf2-KO mice under HFD have an ameliorated metabolic transcriptional program which can partially explain their phenotype, it is not evident which tissue plays the major role in this phenomenon and no information on energy expenditure and respiratory exchange ratio is available from this study. Extension of the study on the HFD-induced obesity model using Keap flox/flox mice would be helpful to better assess the protective effects of genetic Nrf activation in the development of obesity as it is a more physiological model of obesity compared to the aforementioned genetic one
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