Jeong-Eun Park

Anti-obesity effect of kimchi fermented with Weissella koreensis OK1-6 as starter in high-fat diet-induced obese C57BL/6J mice.

In this study, we investigated the anti‐obesity effects of kimchi (Korean traditional fermented vegetable) fermented either without starter culture or with a specific starter culture, Weissella koreensis OK1‐6.

Ethanolic extract of seabuckthorn (Hippophae rhamnoides L) prevents high-fat diet–induced obesity in mice through down-regulation of adipogenic and lipogenic gene expression

Phenolic compounds and flavonoids ameliorate bodyweight, blood glucose, and serum lipid profile. Since seabuckthorn (Hippophae rhamnoides L.) is known as a rich source of isoflavones and flavonoids, we hypothesized that ethanolic extract of seabuckthorn leaves (SL) may have anti-obesity and hypoglycemic effects. To investigate the effect of ethanolic extract of SL, 32 C57BL/6J mice were randomly divided into 4 dietary groups, containing 8 mice in each group: normal diet group; high-fat diet (HD) control group; high-fat diet with SL extract, 500 mg/kg body weight (BW) (SL1) group; and high-fat diet with SL extract, 1000 mg/kg BW (SL2) group. After 13 weeks, it was observed that oral administration of SL extract significantly reduced the energy intake; BW gain; epididymal fat pad weight; hepatic triglyceride, hepatic, and serum total cholesterol levels; and serum leptin levels in the SL groups compared to the HD group. However, differences in serum triglyceride and insulin levels in the SL groups were not significant in comparison to the HD group. The hepatic mRNA expression of peroxisome proliferator-activated receptor (PPAR) α and carnitine palmitoyltransferase 1 along with PPAR-γ were significantly increased in SL groups, whereas the level of acetyl-CoA carboxylase was significantly reduced in SL groups compared to HD group. Our results indicated that SL is effective in preventing BW gain and fat accumulation in the liver; it also reduced adipose tissue mass, hepatic lipid profile, and serum leptin level in the mouse. Together, these observations suggest that SL is a potential agent to study in the management of obesity and related disorders.

Stevia rebaudiana Bertoni extract supplementation improves lipid and carnitine profiles in C57BL/6J mice fed a high‐fat diet

BACKGROUND Stevia (Stevia rebaudiana Bertoni) is a non-caloric natural-source alternative to artificially produced sugar substitutes. This study investigated the effect of stevia extract on lipid profiles in C57BL/6J mice. Forty mice were divided into four groups: N-C (normal diet and distilled water), H-C (high-fat diet and distilled water), H-SC (high fat diet and sucrose, 1 mL kg(-1) per day), and H-SV (high-fat diet and stevia extract, 1 mL kg(-1) per day). RESULTS Body weight gain was significantly higher in the H-SC group than in the H-SV group. Triglyceride concentrations in serum and liver were lower in the H-SV group than in the H-SC group. Serum total cholesterol concentrations were lower in the H-SV and H-C groups compared to the H-SC group. The concentrations of acid-insoluble acylcarnitine (AIAC) in serum were higher in the H-SV group than in the H-C and H-SC groups and the acyl/free carnitine level in liver was significantly higher in the H-SV group than in the N-C group. These results were supported by mRNA expression of enzymes related to lipid metabolism (ACO, PPARalpha, ACS, CPT-I, ACC) assessed by real-time polymerase chain reaction. CONCLUSION These results suggest that the supplementation of stevia extract might have an anti-obesity effect on high-fat diet induced obese mice.

Effects of black adzuki bean (Vigna angularis) extract on proliferation and differentiation of 3T3-L1 preadipocytes into mature adipocytes.

The aim of this work was to investigate the effects of black adzuki bean (BAB) extract on adipocytes, and to elucidate the cellular mechanisms. In order to examine the proliferation of preadipocytes and differentiating adipocytes, cell viability and DNA content were measured over a period of time. Lipid accumulation during cell differentiation and the molecular mechanisms underlying the effects of BAB on the transcriptional factors involved, with their anti-adipogenic effects, were also identified. We observed that BAB exhibits anti-adipogenic effects through the inhibition of proliferation, thereby lowering mRNA expression of C/EBPβ and suppressing adipogenesis during the early stage of differentiation. This, in turn, resulted in a reduction of TG accumulation in a dose- and time-dependent manner. Treating the cells with BAB not only suppressed the adipogenesis-associated key transcription factors PPARγ and C/EBPα but also significantly decreased the mRNA expression of GLUT4, FABP4, LPL and adiponectin. The expression of lipolytic genes like ATGL and HSL were higher in the treatment group than in the control. Overall, the black adzuki bean extract demonstrated an anti-adipogenic property, which makes it a potential dietary supplement for attenuation of obesity.

Lactobacillus plantarum LG42 Isolated from Gajami Sik-Hae Inhibits Adipogenesis in 3T3-L1 Adipocyte

We investigated whether lactic acid bacteria isolated from gajami sik-hae (GLAB) are capable of reducing the intracellular lipid accumulation by downregulating the expression of adipogenesis-related genes in differentiated 3T3-L1 cells. The GLAB, Lactobacillus plantarum LG42, significantly decreased the intracellular triglyceride storage and the glycerol-3-phosphate dehydrogenase (GPDH) activity in a dose-dependent manner. mRNA expression of transcription factors like peroxisome proliferator-activated receptor (PPAR) γ and CCAAT/enhancer-binding protein (C/EBP) α involved in adipogenesis was markedly decreased by the GLAB treatment. Moreover, the GLAB also decreased the expression level of adipogenic markers like adipocyte fatty acid binding protein (aP2), leptin, GPDH, and fatty acid translocase (CD36) significantly. These results suggest that the GLAB inhibits lipid accumulation in the differentiated adipocyte through downregulating the expression of adipogenic transcription factors and other specific genes involved in lipid metabolism.

Lactobacillus brevis OPK-3 isolated from kimchi inhibits adipogenesis and exerts anti-inflammation in 3T3-L1 adipocyte.

BACKGROUND Kimchi is a traditional fermented food in Korea that contains various unique microorganisms. Diverse bacteria are involved in the process of Kimchi fermentation and the healthful advantages; one of the major species is Lactobacillus. We investigated whether lactic acid bacteria isolated from Kimchi (KLAB) are capable of reducing intracellular lipid accumulation by downregulating the expression of adipogenesis and lipogenesis promoting genes in differentiating 3T3-L1 cells. RESULTS KLAB (Lactobacillus brevis OPK-3) mediated dose-dependent inhibition of adipocyte differentiation, intracellular triglyceride accumulation and glycerol-3-phosphate dehydrogenase (GPDH) activity. The expression of transcription factors such as peroxisome proliferator-activated receptor γ and CCAAT/enhancer-binding protein α involved in adipogenesis was markedly decreased by the KLAB treatment. Terminal adipogenic marker, e.g. adipocyte fatty acid binding protein (aP2), lipoprotein lipase, liver X receptor α, leptin and GPDH were significantly downregulated by KLAB treatment compared to untreated control. Moreover, cytokine genes, such as tumor necrosis factor-α and interleukin-6 mRNA expressions level were also decreased, whereas adiponectin mRNA level was upregulated by KLAB. CONCLUSION These results suggest that the KLAB inhibits lipid accumulation in the differentiating adipocyte through downregulating the expression of adipogenic transcription factors and other specific genes involved in lipid metabolism.

G-Aminobutyric acid promotes methionine-choline deficient diet-induced nonalcoholic steatohepatitis

Nonalcoholic steatohepatitis (NASH) is one of the most common liver diseases and a major cause of liver fibrosis worldwide. G-Aminobutyric acid (GABA) is one of the most abundant inhibitory neurotransmitters in the central nervous system. Recently, it has been reported that GABAergic signaling pathways are found in various non-neuronal tissues including the immune system and play a functional role. In the present study, we investigated whether administration of GABA has effects on NASH through its immunomodulatory effects. To test this hypothesis, C57BL/6 mice were fed a methionine-choline-deficient (MCD) diet for 8 weeks. After four weeks into MCD feeding, mice were provided with plain water (control) or water containing 2 mg/mL of GABA for the subsequent 4 weeks. Using this MCD diet-induced NASH model, we found that mice receiving GABA showed more severe steatohepatitis and liver fibrosis than control mice. This increased liver damage was confirmed by higher levels of serum alanine transaminase (ALT) and aspartate aminotransferase (AST) compared to the control group. In accordance with increased liver steatohepatitis, NASH-related and inflammatory gene expression (collagen α1, tissue inhibitor of metalloproteinase-1, TNF-α) in the liver was markedly increased in GABA-treated mice. Furthermore, GABA directly enhanced production of inflammatory cytokines including IL-6 and TNF-α in LPS activated RAW macrophage cells and increased TIB-73 hepatocyte death. Such effects were abolished when GABA was treated with bicuculline, a competitive antagonist of GABA receptors. These results suggest that oral administration of GABA may be involved in changes of the liver immune milieu and conferred detrimental effects on NASH progression.Abstract Nonalcoholic steatohepatitis (NASH) is one of the most common liver diseases and a major cause of liver fibrosis worldwide. Γ-Aminobutyric acid (GABA) is one of the most abundant inhibitory neurotransmitters in the central nervous system. Recently, it has been reported that GABAergic signaling pathways are found in various non-neuronal tissues including the immune system and play a functional role. In the present study, we investigated whether administration of GABA has effects on NASH through its immunomodulatory effects. To test this hypothesis, C57BL/6 mice were fed a methionine–choline-deficient (MCD) diet for 8 weeks. After four weeks into MCD feeding, mice were provided with plain water (control) or water containing 2 mg/mL of GABA for the subsequent 4 weeks. Using this MCD diet-induced NASH model, we found that mice receiving GABA showed more severe steatohepatitis and liver fibrosis than control mice. This increased liver damage was confirmed by higher levels of serum alanine transaminase (ALT) and aspartate aminotransferase (AST) compared to the control group. In accordance with increased liver steatohepatitis, NASH-related and inflammatory gene expression (collagen α1, tissue inhibitor of metalloproteinase-1, TNF-α) in the liver was markedly increased in GABA-treated mice. Furthermore, GABA directly enhanced production of inflammatory cytokines including IL-6 and TNF-α in LPS activated RAW macrophage cells and increased TIB–73 hepatocyte death. Such effects were abolished when GABA was treated with bicuculline, a competitive antagonist of GABA receptors. These results suggest that oral administration of GABA may be involved in changes of the liver immune milieu and conferred detrimental effects on NASH progression.