Abstract
In recent decades, the prevalence of obesity has risen dramatically worldwide among all age groups. Obesity is characterized by excess fat accumulation and chronic low-grade inflammation. The adipose tissue functions as a metabolically active endocrine organ secreting adipokines. A novel duo of adipokines, the anti-inflammatory secreted frizzled-related protein 5 (Sfrp5) and the proinflammatory wingless type mouse mammary tumor virus (MMTV) integration site family member 5A (Wnt5a), signal via the non-canonical Wnt pathway. Recent evidence suggests that Sfpr5 and Wnt5a play a key role in the pathogenesis of obesity and its metabolic complications. This review summarizes the current knowledge on the novel regulatory system of anti-inflammatory Sfrp5 and pro-inflammatory Wnt5a, and their relation to obesity and obesity-related complications. Future studies are required to investigate the potential role of Sfrp5 and Wnt5a as biomarkers for monitoring the response to lifestyle interventions and for predicting the development of cardiometabolic risk factors. These adipokines may also serve as novel therapeutic targets for obesity-related disorders.
Highlights
Obesity has emerged as a pandemic of the 21st century, and its global prevalence has nearly tripled since 1975 [1]
secreted frizzled-related protein 5 (Sfrp5) is an adipokine which may play a protective role against obesity-related insulin resistance and T2D by binding to Wnt5a and improving insulin sensitivity
This review summarizes the current evidence on the emerging role of Sfrp5 and Wnt5a in the pathogenesis of obesity, T2D and cardiovascular disease
Summary
Obesity has emerged as a pandemic of the 21st century, and its global prevalence has nearly tripled since 1975 [1]. Excess free fatty acids lead to ectopic lipid accumulation and contribute towards the development of obesity-related metabolic disturbances, especially insulin resistance [29] This dysregulation is accompanied by an increase in the secretion of various proinflammatory chemokines and cytokines by macrophages, causing chronic low-grade inflammation [29,30], which in turn triggers a multitude of complications [31]. It is involved in the process of maturation of fat cells, as the Sfrp gene is a target of the transcription factor PPARγ [48] It exerts vasodilating actions by regulating nitric oxide production via inhibiting the WNT5A/JNK pathway in endothelial cells [49]. Wnt5a and Sfrp appear to be critical players in the regulation of systemic inflammation in obesity and glucose homeostasis, as well as mediators between adipose tissue and other key metabolic organs, including the liver and the pancreas
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