Metabolic Syndrome can be defined as a cluster of abnormalities which includes obesity, dyslipidemia, hypertension, and insulin resistance. The intricate connections between genetic and environmental variables are involved in the development of metabolic syndrome (MetS). Nuclear receptors (NR), a family of transcription factors, are the key participants in onset and progression of MetS because their major mechanism of action is to modulate various metabolic pathways. The main characteristic features of MetS include abnormal distribution of adipose tissue, aberrant lipid profiles, decreased glucose tolerance, and inflammation, and these all develop due to dysregulation of NR signaling. This review is an attempt to understand the principles of molecular mechanisms and functions of nuclear receptors that can be utilized in the treatment of MetS, because numerous critical processes, such as adipocyte development, lipid metabolism, glucose homeostasis, and inflammation, are strongly mediated by nuclear receptors, e.g. FXR, LXR, GR, and PPARs. In addition, understanding how nuclear receptors interact with other signaling pathways may lead to findings of new therapeutic targets for MetS. Understanding specific methods by which nuclear receptors affect metabolic pathways would further our knowledge of the pathophysiology of MetS, and open the door to future development of novel treatment approaches.
Singh et al. (Sat,) studied this question.