Selenate Prevents Adipogenesis through Induction of Selenoprotein S and Attenuation of Endoplasmic Reticulum Stress.
Choon Young KimKee-Hong KimPublished in: Molecules (Basel, Switzerland) (2018)
The conversion of preadipocytes to adipocytes (adipogenesis) is a potential target to treat or prevent obesity. Selenate, an inorganic form of selenium, elicits diverse health benefits, mainly through its incorporation into selenoproteins. The individual roles of selenium and certain selenoproteins have been reported. However, the effects of selenate treatment on selenoproteins in adipocytes are unclear. In this study, the effects of selenate pretreatment on selenoprotein and endoplasmic reticulum (ER) stress during adipogenesis were examined in vitro. The selenate pretreatment dose-dependently suppressed the adipogenesis of 3T3-L1 preadipocytes. The selenate pretreatment at 50 μM for 24 h almost completely suppressed adipogenesis without cytotoxic effects. The expression of the adipogenic genes peroxisome proliferator-activated receptor gamma, CCAAT-enhancer binding protein alpha, and leptin was suppressed by selenate. This pretreatment also upregulated selenoprotein S (SEPS1), an ER resident selenoprotein that reduces ER stress, and prevented dexamethasone-induced SEPS1 degradation during the early stage of adipogenesis. The selenate-inhibited adipogenesis was associated with an attenuation of ER stress. The expression of the ER stress marker genes was upregulated during the early stage of differentiation, whereas the selenate pretreatment suppressed the mRNA expression of the XBP1 and C/EBP homologous protein. The collective data suggest a preventive role of selenate and SEPS1 in adipogenesis, and support a novel dietary approach to prevent obesity.
Keyphrases
- high fat diet induced
- binding protein
- early stage
- insulin resistance
- endoplasmic reticulum stress
- endoplasmic reticulum
- poor prognosis
- metabolic syndrome
- adipose tissue
- type diabetes
- healthcare
- public health
- genome wide
- weight loss
- dna methylation
- induced apoptosis
- physical activity
- radiation therapy
- gene expression
- quality improvement
- dna damage
- oxidative stress
- amino acid
- weight gain
- small molecule
- risk assessment
- stress induced
- data analysis
- transcription factor
- lymph node
- genome wide analysis
- diabetic rats