Journal of the Society of Cosmetic Scientists of Korea
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v.48
no.4
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pp.331-342
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2022
Obesity is one of the metabolic diseases caused by excessive differentiation and accumulation of adipose tissue due to an imbalance between energy intake and consumption. In this study, we investigated the anti-obesity effect of SliMax, a natural-derived 6 compounds mixture, by using 3T3-L1 cells. As a result, SliMax showed the inhibitory effect on adipocyte differentiation through down-regulation of the PPARγ and C/EBPα expression, which are known to regulate the late adipogenesis stage. In the process of lipolysis on differentiated 3T3-L1 cells, SliMax accelerated decomposition of large-sized unilocular lipid droplet into numerous small-sized multilocular lipid droplets through up-regulation of the expression of lipolysis-related proteins ATGL and HSL. Finally, in order to confirm the effect of SliMax on induction of brown adipocyte, the expression of UCP-1 and the amount of mitochondria were confirmed by immunofluorescent staining, and as a result, SliMax increased the expression of UCP-1 and the amount of mitochondria in fat cells. Taken together, those results suggest that SliMax, a naturally-derived mixture, have a potential to be anti-obesity agent through exerting inhibitory effect on the formation of lipid droplet by suppression of adipogenesis and stimulation of lipolysis, and browning effect associated with generation of heat energy and energy consumption.
Xin, Li;Hao, Zhang;Yong, Wang;Yanyan, Li;Youli, Wang;Jiangjiang, Zhu;Yaqiu, Lin
Animal Bioscience
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v.36
no.1
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pp.144-155
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2023
Objective: Adipocyte differentiation is regulated by a variety of functional genes and noncoding RNAs. However, the role of miRNAs in lipid deposition of goat white adipose tissue is still unclear. Therefore, this study revealed the miRNA expression profile in goat subcutaneous adipocytes by sRNA-seq. Methods: The miRNA expressed in goat subcutaneous preadipocytes and the mature adipocytes were sequenced by sRNA-seq. The differentially expressed miRNAs (DEm) were screened and gene ontology (GO) and Kyoto encyclopedia for genes and genomes (KEGG) analyses were performed. Gain-of-function and loss-of-function combined with oil red O staining, Bodipy staining, and quantitative reverse-transcription polymerase chain reaction (qPCR) were utilized to determine the effect of miR-133a-3p on adipocyte differentiation. Results: A total of 218 DEm were screened out. The target genes of these DEm were significantly enriched in GO items such as biological regulation and in KEGG terms such as FAK signaling pathway and MAPK signaling pathway. qPCR verified that the expression trend of miRNA was consistent with miRNA-seq. The gain-of-function or loss-of-function of miR-133a-3p showed that it promoted or inhibited the accumulation of lipid droplets, and CCAAT enhancer binding protein α (C/EBPα) and C/EBPβ were extremely significantly up-regulated or down-regulated respectively (p<0.01), the loss-of-function also led to a significant down-regulation of peroxisome proliferator activated receptor gamma (PPARγ) (p<0.01). Conclusion: This study successfully identified miRNAs expression patterns in goat subcutaneous adipocytes, and functional identification indicates that miR-133a-3p is a positive regulator of the differentiation process of goat subcutaneous adipocytes. Our results lay the foundation for the molecular mechanism of lipid deposition in meat-source goats from the perspective of miRNA.
Roh, Jong Seong;Lee, Hye Rim;Ahn, Ye Ji;Yoon, Mi Chung;Shin, Soon Shik
The Korea Journal of Herbology
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v.29
no.2
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pp.23-31
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2014
Objectives : This study was undertaken to verify the effects of Massa Medicata Fermentata (MMF) on nonalcoholic fatty liver disease (NAFLD) using high fat diet-fed male mice. Methods : Fifty four male C57BL/6N mice (age matched) were used for all experiments. Nine standard chow diet-fed mice were used as normal group and forty five high fat diet-fed obese mice were randomly divided into 5 groups: control, atorvastatin-10mg/kg, MMF(1)-62.5mg/kg, MMF(2)-125mg/kg and MMF(3)-250mg/kg. After all groups were treated with several kinds of diets for 8 weeks, we measured body weight gain, adipose tissue weights, plasma lipid and glucose metabolism, visceral organ weights, histological analysis for liver on the mice. Results : MMF-treated mice had lower body weight gain compared with controls. Among MMF-treated mice, the effect was magnified in MMF(2). MMF(3)-treated mice had lower blood plasma total cholesterol (TC) and glucose level compared with controls. MMF decreased hepatic lipid accumulation, liver fibrosis and liver inflammation of mice compared with controls. The effects was maximized in MMF(2) and atorvastatin. Blood plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT), ${\gamma}$-glutamyltransferase (${\gamma}$-GT) concentrations tends to be decreased by MMF compared with controls. Blood plasma AST, ALT, ${\gamma}$-GT concentrations and organ weights were not changed by MMF, indicating that all three kinds of MMF do not show any hepatotoxicity. Conclusions : These results suggest that MMF improves NAFLD by reducing body weight gain, hepatic lipid accumulation, liver fibrosis, liver inflammation.
Ahn, Ye Ji;Yoon, Ki Hyeon;Jo, Ju Heum;Jang, Du Hyon;Jung, Yang Sam;Kim, Jong Hoon;Kim, Byeong Chul;Seok, Hoa Jun;Yoo, Jae Sang;Ku, Ja Ryong;Yoon, Michung;Shin, Soon Shik
The Korea Journal of Herbology
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v.29
no.2
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pp.47-54
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2014
Objectives : This study was undertaken to verify the effect of Gangjihwan(Di-fatty, DF) composed with Pakistani Ephedra Herba on nonalcoholic fatty liver disease(NAFLD) using high fat diet-fed male mice. Method : Eight-week old C57BL/6N mice were used for all experiments. Standard chow diet-fed mice were used as normal group and high fat diet-fed NAFLD mice were randomly divided into 5 groups: control, atorvastatin, DF(1), DF(2) and DF(3). After 8 weeks, mice were treated with water, atorvastatin(10mg/kg) and DF(40, 80, 160mg/kg) for 8 weeks. And we investigated body weight gain, plasma lipid and glucose metabolism, histological analysis for liver on the mice. Results : Compared with controls, DF-treated mice had very significantly lower body weight gain and lower visceral adipose tissue weight, the magnitudes of which were prominent in DF(3). Consistent with their effects on body weight gain, DF-treated mice had lower blood total cholesterol and triglyceride level compared with controls. Consistent with their effects on body weight gain and blood plasma lipid level, DF-treated mice had lower liver weight and hepatic lipid accumulation of DF-treated groups was significantly decreased than control group. Also Blood plasma AST, ALT and ${\gamma}$-GT concentration were not changed by DF, and these results may indicate DF do not show any toxic effects. Conclusions : These results suggest that DF effectively improves NAFLD. DF reduces liver weight and prevents lipid accumulation of hepatocyte by reducing body weight gain and modulating blood plasma lipid metabolism levels.
Objectives : We investigated the effects of gambigyeongsinhwan(GGH)(1) on body weight and non-alcoholic fatty liver disease(NAFLD) examined whether blood total cholesterol, LDL-cholesterol, free fatty acid and triglyceride levels and hepatic lipid accumulation are inhibited by it in high fat diet-fed obese male mice. Methods : 8 weeks old, high fat diet-fed obese male mice were divided into 5 groups: C57BL/6N normal, control, GGH(1)-1, GGH(1)-2 and GGH(1)-3. After mice were treated with GGH(1) for 8 weeks, we measured body weight gain, food intake, feeding efficiency ratio, fat weight, plasma ALT, leptin and lipid levels. We also did histological analysis for liver and fat on the mice. Results : Compared with controls, GGH(1)-treated mice had lower body weight gain and adipose tissue weight, the magnitudes of which were prominent in GGH(1)-3. Compared with controls, GGH(1)-treated mice had lower feeding efficiency ratio and blood leptin level, the magnitudes of which was prominent in GGH(1)-3. Compared with controls, GGH(1)-treated mice had lower blood plasma total cholesterol, LDL-cholesterol, free fatty acid and triglyceride levels. Compared with controls, GGH(1)-3 treated mice had lower blood plasma ALT concentration. Consistent with their effects on body weight gain, the size of adipocytes were significantly decreased by GGH(1), whereas the adipocyte number per unit area was significantly increased, suggesting that GGH(1) decreased the number of large adipocytes. Hepatic lipid accumulation was decreased by GGH(1). Conclusions : In conclusion, these results suggest that GGH(1) exhibits anti-obesity effects through the modulation of feeding efficiency ratio and plasma obesity parameters. Moreover, it seems that GGH(1) also contributes to improve NAFLD through the regulation of plasma ALT and hepatic triglyceride accumulation.
Objectives : The purpose of this study was to determine the anti-obesity effect and molecular mechanism of YY312, a herbal extract composed of Imperatae Rhizoma, Citri Unshius Pericarpium Immaturus, and Evodiae Fructus, on a high-fat diet-induced animal model and on 3T3-L1 cells. Methods : C57BL/6 mice were fed for 6 weeks with a normal diet or a high-fat diet (HFD). Then they orally administered daily with 300 mg/kg YY312 for next 10 weeks. Body weight and food consumption were recorded weekly and daily, respectively. Tissue weights, serum lipid, and glucose levels were analyzed at the end of the study. Additionally, the effects of YY312 on adipocyte differentiation in 3T3-L1 cells were examined. After differentiating 3T3-L1 cells were treated with YY312, Oil-red O staining, RT-PCR, and Western blotting were performed for lipid accumulation, mRNA expression of adipogenesis gene, and AMP-activated protein kinase (AMPK) phosphorylation, respectively. Results : YY312-administered mice showed a significant reduction of body weights and abdominal adipose tissue weights. YY312 also reduced the serum levels of triglycerides and total cholesterol, compared with the HFD group. Treatment with YY312 inhibited lipid accumulation and blocked expression of adipogenic transcription factors and lipogenesis genes, including peroxisome proliferator-activated receptor ${\gamma}$, CCAT/enhancer binding protein ${\alpha}$ and fatty acid synthase. YY312 increased AMPK phosphorylation in 3T3-L1 adipocytes. Conclusions : This study showed that herbal extract YY312 has an anti-obesity effect in vitro and in vivo. Thus, YY312 could be developed as a supplement for reduction of body weight gain induced by an HFD.
We investigated the serum cholesterol and visceral fat lowering effects of Momordica charanatia (MC) and Withania somnifera (WS) extracts in high-fat diet (HFD)-fed mice. Combination of fermented MC and WS extracts (FMCWS) as well as that of non-fermented extracts (MCWS) were orally administered to HFD-induced obese mice along with the HFD supplementation for 8 weeks. During the experiment, body weight, food intake, and levels of total cholesterol, triglyceride and HDL-cholesterol were analyzed. Body weight and the levels of total cholesterol and triglycerides were significantly increased in the HFD-fed mice compared with the normal control (NC) group. However, supplementation of the extracts showed a tendency to reduce body weight gain and suppressed the levels of total cholesterol and triglyceride with the increment of HDL-cholesterol levels. Abdominal fat weight was significantly increased in the HFD group, and the size of adipocytes within the epididymal adipose tissue was markedly expanded compared with the NC group. However, in the FMCWS and MCWS groups, the abdominal fat weight was significantly reduced and the sizes of the adipocytes were noticeably diminished compared with those of the HFD-fed mice. Moreover, the deposition of giant vesicular fat cells observed in the liver tissue of the HFD group was prominently reduced in these groups. These results indicate that the combination of extracts from MC and WS tends to have potent synergic effects in reducing body weight gain as well as significantly lowering the visceral fat and the serum lipid levels, and thus improving anti-obesity efficacy in HFD-induced obese mice.
Kim, Ye-Seul;Kim, Ha-Rim;Park, Eun-Hee;Song, Young-Eun;Kim, Chang-Su;Ha, Won-Bae;Woo, Hyeon-Jun;Han, Yun-Hee;Lee, Jung-Han
Journal of Korean Medicine Rehabilitation
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v.32
no.4
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pp.1-8
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2022
Objectives This study is to investigate the effects and mechanisms of Gastrodia elata extract (GEE) on the high-fat diet-induced obesity model. Methods C57BL/6 mice were randomly assigned into 5 groups (n=10). Control group was fed normal diet (ND). Obesity group was fed 60% high fat diet (HFD). The other three groups were fed HFD with 100, 200, 500 mg/kg GEE. After five weeks, body weight, liver and epididymal fat weight, triglyceride concentration in liver and serum, sterol regulatory element-binding protein-1 (SREBP-1), acetyl-CoA carboxylase (ACC), fatty acid synthase, peroxisome proliferator-activated receptor 𝛾 (PPAR-𝛾), CCAAT/enhancer binding protein 𝛼 (C/EBP-𝛼) expression level, insulin concentration in serum were measured. Results The GEE (100, 200, and 500 mg/kg)-treated animals exhibited substantial decreases in body mass, liver weight and epididymal white adipose tissue collate to the HFD-fed group. GEE treatment also reduced hepatic and serum triglyceride level. Furthermore, GEE treatment significantly inhibited adipogenesis in the GEE group by reducing the protein expression of SREBP-1, ACC and the messenger RNA expression of PPAR𝛾, C/EBP-𝛼, which are adipocyte differentiation-related genes. Conclusions These research outcomes recommend that GEE is possibly valuable for the prevention of HFD-induced obesity via modification of various pathways related with adipogenesis and adipocyte differentiation.
Background: Hepatic lipid disorder impaired mitochondrial homeostasis and intracellular redox balance, triggering development of non-alcohol fatty liver disease (NAFLD), while effective therapeutic approach remains inadequate. Ginsenosides Rc has been reported to maintain glucose balance in adipose tissue, while its role in regulating lipid metabolism remain vacant. Thus, we investigated the function and mechanism of ginsenosides Rc in defending high fat diet (HFD)-induced NAFLD. Methods: Mice primary hepatocytes (MPHs) challenged with oleic acid & palmitic acid were used to test the effects of ginsenosides Rc on intracellular lipid metabolism. RNAseq and molecular docking study were performed to explore potential targets of ginsenosides Rc in defending lipid deposition. Wild type and liver specific sirtuin 6 (SIRT6, 50721) deficient mice on HFD for 12 weeks were subjected to different dose of ginsenosides Rc to determine the function and detailed mechanism in vivo. Results: We identified ginsenosides Rc as a novel SIRT6 activator via increasing its expression and deacetylase activity. Ginsenosides Rc defends OA&PA-induced lipid deposition in MPHs and protects mice against HFD-induced metabolic disorder in dosage dependent manner. Ginsenosides Rc (20mg/kg) injection improved glucose intolerance, insulin resistance, oxidative stress and inflammation response in HFD mice. Ginsenosides Rc treatment accelerates peroxisome proliferator activated receptor alpha (PPAR-α, 19013)-mediated fatty acid oxidation in vivo and in vitro. Hepatic specific SIRT6 deletion abolished ginsenoside Rc-derived protective effects against HFD-induced NAFLD. Conclusion: Ginsenosides Rc protects mice against HFD-induced hepatosteatosis by improving PPAR-α-mediated fatty acid oxidation and antioxidant capacity in a SIRT6 dependent manner, and providing a promising strategy for NAFLD.
This study was designed to evaluate the effects of fructose(F) or sucrose(S) and guar gum intake on carbohydrate and lipid metabolism in 15-week-old male Goto-Kakizaki(GK) rats. Fifty rats were randomly assigned to 5 groups which were different in carbohydrate(25% of carbohydrate) and fiber(5% w/w) sources. The carbohydrate(CHO) sources of each group were comstarch(control group, 100% of CHO), fructose with cellulose(F), fructose with guar gum(FG), sucrose with cellulose(S), and sucrose with guar gum(SG). Each group was fed exterimental diet for 4 weeks. We measured food intake, body weight gain, adipose tissues weight and organs weight. We conducted oral glucose tolerance test(OGTT) and measured plasma insulin concentration to examine carbohydrate metabolism. To evaluate lipid metabolism, we measured the lipid profile of plasma, liver and feces. Food intake and weight gain of FG or SG groups tended to be less than those of F or S groups. Perirenal and epididymal fat pad weights of SG group were significantly lower than those of S group and those of FG group tended to be lower than those of F group. In OGTT, blood glucose values of F or S groups were significantly higher than those of C group, and FG or SG groups tended to be lower than those of F or S groups during the experimental time. The area under the curve(AUC) of C group was significantly highest among the groups, AUC and plasma insulin concentration of FG or SG groups tended to be lower than those of F or S groups. Plasma and hepatic triglyceride (TG) of FG and SG groups were significantly lower than those of F and S groups, plasma and hepatic total lipid(TL) and total cholesterol(TC) of FG and SG groups tended to be lower than those of F and S groups. Fecal TL, TG and TC of FG or SG groups tended to be higher than those of F and S groups. In conclusion, intake of guar gum should improve carbohydrate and lipid metabolism in partial substitution of fructose or sucrose for cornstarch in GK rats.
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