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Abstract
Selenium (Se) homeostasis is tightly related to carbohydrate and lipid metabolism, but its possible roles in obesity development and in adipocyte metabolism are unclear. The objective of the present study is to review the current data on Se status in obesity and to discuss the interference between Se and selenoprotein metabolism in adipocyte physiology and obesity pathogenesis. The overview and meta-analysis of the studies on blood Se and selenoprotein P (SELENOP) levels, as well as glutathione peroxidase (GPX) activity in obese subjects, have yielded heterogenous and even conflicting results. Laboratory studies demonstrate that Se may modulate preadipocyte proliferation and adipogenic differentiation, and also interfere with insulin signaling, and regulate lipolysis. Knockout models have demonstrated that the selenoprotein machinery, including endoplasmic reticulum-resident selenoproteins together with GPXs and thioredoxin reductases (TXNRDs), are tightly related to adipocyte development and functioning. In conclusion, Se and selenoproteins appear to play an essential role in adipose tissue physiology, although human data are inconsistent. Taken together, these findings do not support the utility of Se supplementation to prevent or alleviate obesity in humans. Further human and laboratory studies are required to elucidate associations between Se metabolism and obesity.
Highlights
Selenium (Se) is a metalloid discovered by the Swedish chemist Jöns Jakob Berzelius in 1817 and recognized as an essential trace element in higher animals in 1957 [1]
In patients with visceral obesity plasma Se levels significantly correlated with high density lipoprotein cholesterol (HDL-C) and fatty acid binding protein 4 (FABP4), whereas in metabolic syndrome (MetS) plasma Se levels were inversely associated with circulating macrophage chemoattractant protein 1 (MCP-1)
Selenoprotein M gene (Selenom)-KO was associated with increased weight gain and adipose tissue accumulation at least partially associated with hypothalamic leptin resistance, being indicative of the potential involvement of this selenoprotein into central regulation of energy metabolism [220]
Summary
Selenium (Se) is a metalloid discovered by the Swedish chemist Jöns Jakob Berzelius in 1817 and recognized as an essential trace element in higher animals in 1957 [1]. Physiological functions of Se are mainly mediated through Se-containing proteins, selenoproteins, containing Se in the form of selenocysteine [2], inorganic Se may possess direct biological activity [3]. Selenoproteins, such as glutathione peroxidases (GPXs) and thioredoxin reductases (TXNRDs), were initially recognized as antioxidants. Gut microbiota may mediate the effects of dietary Se on Se status of the host through modulation of selenoprotein metabolism [15]. Alteration in gut microbiota in a number of intestinal (inflammatory bowel disease, Crohn’s disease, colon cancer) and metabolic (e.g., obesity) diseases may modify dietary Se bioavailability and status. Since units of measurement may differ across the selected studies, we computed the standardized mean differences (SMD) and corresponding 95% confidence intervals (CIs), using a random-effect model to account for heterogeneity (I2) in study-specific results
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