According to the Centers for Disease Control (CDC), about 1 in 5 children and 1 in 3 adults struggle with obesity. There are a number of contributing factors that can explain this, including low intake of healthy foods, genetic predispositions, lack of exercise, and poor access to fresh fruits and vegetables.
Whatever the reason, nutritional researchers are keen on finding ways to help stop excess weight from accumulating. One potential answer may be the mineral selenium.
Selenium is found naturally in foods, including tuna, liver, oysters, pork, clams, and Brazil nuts. But depending on your diet, getting selenium consistently, and at meaningful levels may be a challenge.
This study found that a form of selenium called selenite decreased levels of inflammatory markers, including COX-2, which can be both a cause and reaction to being overweight. It also boosted levels of important natural antioxidants, including glutathione peroxidase and selenoproteins.
But most intriguingly, it prevented the formation of fat cells (adipogenesis) and reduced the accumulation of fat cells in an animal study.
Certainly, one nutrient in isolation isn’t the only way to address a struggle with being overweight or obese, but this study definitely points to the great potential for minerals to help in the fight.
El-Magd NFA, Barbosa PO, Nick J, Covalero V, Grignetti G, Bermano G. Selenium, as selenite, prevents adipogenesis by modulating selenoproteins gene expression and oxidative stress-related genes. Nutrition. 2021; 111424, ISSN 0899-9007, https://doi.org/10.1016/j.nut.2021.111424.
Objective: This study aimed to assess the effect of the micronutrient selenium, as inorganic selenite, on adipocytes differentiation and to identify underlying molecular mechanisms, while advancing understanding of basic cellular mechanisms associated with adipogenesis.
Methods: 3T3-L1 murine preadipocytes were used to investigate the effect of sodium selenite (Na2SeO3) on cell viability (MTT assay) in preadipocytes, lipid accumulation (Oil Red O staining) and intracellular reactive oxygen species (ROS, NBT assay) in mature adipocytes, in addition to explore molecular mechanisms via gene expression analyses (RT-qPCR), pre and post differentiation.
Results: Selenite (100, 200, 400nM) significantly decreased lipid accumulation during differentiation compared to untreated adipocytes (P<0.05, 0.001, 0.01, respectively). Pre-adipocytes exposure (48h) to selenite caused an increase in glutathione peroxidase 1 (Gpx1) gene expression in a dose-dependent manner. Adipogenesis significantly increased intracellular ROS levels (P<0.05) while decreasing gene expression of antioxidant enzymes (Gpx1, P<0.05) and significantly increasing gene expression of regulators of lipid catabolism (type II iodothyronine deiodinase, Dio2, P<0.01) and of markers of differentiation (e.g. selenium-binding protein 1, Selenbp1, peroxisome proliferator activated receptor gamma, Pparg, CCAAT/enhancer binding protein alpha, Cebpa, and fatty acid binding protein 4, Fabp4) compared to pre-adipocytes (P<0.01, 0.01, 0.01 and 0.001, respectively). Selenite exposure (200nM) caused a significant increase in Gpx1, selenoprotein W (Selenow), selenoprotein P (Selenop) gene expression in differentiated adipocytes compared to untreated ones (P<0.01, 0.001, 0.05, respectively) with a significant decrease in heme oxygenase 1 (Ho-1), cyclooxygenase 2 (Cox2), Dio2 and Fabp4 gene expression (P<0.001, 0.05, 0.05 and 0.01, respectively).
Conclusions: Selenium, as selenite, prevented adipogenesis through increasing antioxidant selenoproteins expression, leading to decreased inflammatory markers and, subsequently, to decrease in differentiation and lipid deposition. These findings, if demonstrated in vivo, could provide valuable data for novel dietary approaches to prevent obesity.
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