Selenium is an essential trace mineral for various functions in the body and is known as an antioxidant. To evaluate the anti-obesity effect of sodium selenite (SS), we examined the expressions of epigenetic regulatory enzymes and the anti-adipogenic and lipogenic effects of SS in MDI-induced 3T3-L1 preadipocytes. SS significantly inhibited protein arginine methyltransferase 5 (PRMT5) and histone acetyltransferase (HAT) activity compared with a control, epigallocatechine gallate. SS also attenuated lipid accumulation and triglyceride formation in 3T3-L1 adipocytes. In addition, SS decreased the protein and mRNA levels of adipogenic transcription factors such as peroxisome proliferator-activated receptor gamma, CCAAT/enhaner binding protein alpha. SS effectively suppressed the mRNA expressions of the fatty acid synthase and ATP citrate lyase known as the lipogenic markers and the P300/CBP-associated factor known as an epigenetic regulatory marker in 3T3-L1 adipocytes. Consequently, the anti-obesity effect of SS is likely attributed to the inhibition of PRMT5 and HAT activity.

BACKGROUND/OBJECTIVES Epigenetic regulation by nutrients can influence the development of specific diseases. This study sought to examine the effect of individual nutrients and nutrient families in the context of preventing chronic metabolic diseases via epigenetic regulation. The inhibition of lipid accumulation and inflammation by nutrients including proteins, lipids, vitamins, and minerals were observed, and histone acetylation by histone acetyltransferase (HAT) was measured. Correlative analyses were also performed. MATERIALS/METHODS Nutrients were selected according to information from the Korean Ministry of Food and Drug Safety. Selected nutrient functionalities, including the attenuation of fatty acid-induced lipid accumulation and lipopolysaccharide-mediated acute inflammation were evaluated in mouse macrophage Raw264.7 and mouse hepatocyte AML-12 cells. Effects of the selected nutrients on in vitro HAT inhibition were also evaluated. RESULTS Nitric oxide (NO) production correlated with HAT activity, which was regulated by the amino acids group, suggesting that amino acids potentially contribute to the attenuation of NO production via the inhibition of HAT activity. Unsaturated fatty acids tended to attenuate inflammation by inhibiting NO production, which may be attributable to the inhibition of in vitro HAT activity. In contrast to water-soluble vitamins, the lipid-soluble vitamins significantly decreased NO production. Water- and lipid-soluble vitamins both exhibited significant inhibitory activities against HAT. In addition, calcium and manganese significantly inhibited lipid accumulation, NO production, and HAT activity. CONCLUSIONS Several candidate nutrients and their family members may have roles in the prevention of diseases, including hepatic steatosis and inflammation-related diseases (i.e., nonalcoholic steatohepatitis) via epigenetic regulation. Further studies are warranted to determine which specific amino acids, unsaturated fatty acids and lipid-soluble vitamins or specific minerals influence the development of steatosis and inflammatory-related diseases.

This study aimed to assess the anti-inflammatory activity and the mechanism of anti-inflammatory action of barley sprout (Hordeum vulgare L.). Barley sprout powder (BSP), barley sprout ethanol extract (BSE), and barley sprout water extract (BSW) were prepared, and the inhibitory effects of the samples on nitric oxide (NO) production were evaluated. The results showed that the inhibitory activity of BSE and BSW on NO production was greater compared to BSP. Among the active compounds found in barley sprouts, luteolin exhibited greater inhibition of NO production and histone acetyltransferase (HAT) activity compared to the other compounds. Luteolin significantly (P<0.05) attenuated lipopolysaccharide (LPS)-mediated inflammatory mediators, including interleukin-6, tumor necrosis factor-α, inducible nitric oxide synthase, and cyclooxygenase-2 in RAW264.7 cells. Luteolin also significantly inhibited in vitro specific HATs (p300, CBP, PCAF) as well as total HAT, which was also observed in the nuclear fraction of LPS-treated RAW264.7 cells. The anti-inflammatory activity of luteolin was attributed to total and specific HAT inhibition. Collectively, the anti-inflammatory activity of barley sprouts could be attributed to luteolin via HAT inhibition.