• 한방비만학회지
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• 제22권2호
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• pp.102-114
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• 2022

Objectives: We investigated the effects of Allii Fistulosi Bulbus (AFB) on high fat diet (HFD)-induced obesity in mice and the regulation of energy metabolism in muscle tissues of mice. Methods: The C57BL/6 mice (6 weeks, male) were fed a HFD for 8 weeks and then administrated with AFB extract at 500 mg/kg (p.o.) once daily for 4 weeks. The body weight (BW), muscle weight, calorie intake, fasting blood glucose (FBG) and serum glucose, insulin, and low-density lipoprotein-cholesterol (LDL-C) levels were measured in mice. It was also observed the histological changes of pancreas, liver, and fat tissues with hematoxylin and eosin staining. It was investigated the phosphorylation of insulin receptor substrate 1 (IRS-1), Ser/Thr kinase (AKT), and adenosine monophosphate-activated protein kinase (AMPK), and the expression of phosphoinositide 3-kinase, glucose transporter type 4 (GLUT4), and sirtuin1 (Sirt1) in gastrocnemius tissues by western blot, respectively. Results: The increases of BWs, calorie intakes and FBG levels in obesity mice were decreased significantly by the administration of AFB extract. The AFB extract administration was reduced significantly serum levels of glucose, insulin, and LDL-C in obesity mice. The AFB extract inhibited lipid accumulation in liver tissues, hyperplasia of pancreatic islets, and enlargement of fat tissues in obesity mice. The phosphorylation of IRS-1 and AKT was increased significantly in muscle tissues and AMPK phosphorylation and the GLUT4 and Sirt1 expression were decreased significantly in muscle tissues after the AFB administration. Conclusions: Our study indicates that AFB extract improves symptoms of obesity through regulation of energy regulating proteins in muscle tissues.

• 대한의생명과학회지
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• 제16권3호
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• pp.151-159
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• 2010

The peroxisome proliferator-activated receptor $\alpha$ (PPAR$\alpha$) is a nuclear transcription factor that plays a central role in lipid metabolism and obesity. Exercise also is a powerful modifier of the manifestations of the lipid metabolism and obesity in animal models and humans with obesity and metabolic syndrome. However, effects of exercise on lipid metabolism and obesity in normal-weight younger female subjects, having functional ovaries and not metabolic disease, remain unexplained. To explore the effects of exercise on the development of obesity and its molecular mechanism in high fat diet-fed female C57BL/6J mice, we experimented the effects of swim training on body weight, adipose tissue mass, serum lipid levels, morphological changes of adipocytes and the expression of PPAR$\alpha$ target genes involved in fat oxidation in skeletal muscle tissue of female C57BL/6J mice. Swim-trained mice had significantly decreased body weight, adipose tissue mass, serum triglycerides compared with female control mice. Histological studies showed that swim training significantly decreased the average size of adipoctyes in parametrial adipose tissue. Swim training did not affect the expression of PPAR$\alpha$ mRNA in skeletal muscle. Concomitantly, swim training did not increase mRNA levels of PPAR$\alpha$ target genes responsible for fatty acid $\beta$-oxidation, such as carnitine palmitoyltransferase 1, medium chain acyl-CoA dehydrogenase, enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase, and thiolase in skeletal muscle. In conclusion, these results indicate that swim training regulates lipid metabolism and obesity in high fat diet fed-female mice although swim training did not increase mRNA levels of PPAR$\alpha$ target genes involved in fatty acid $\beta$-oxidation in skeletal muscle, suggesting that swim training may prevent obesity and improve fitness through other mechanisms in female with ovaries, not through the activation of skeletal muscle PPAR$\alpha$.

• 동의생리병리학회지
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• 제19권4호
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• pp.1055-1061
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• 2005

In this study, the aim was to investigate the effect of Mahwangpohang-tang on the expression of obesity-related genes and cytokines in high fat diet induced obesity mice. In order to investigate the effects of Mahwangpohang-tang(MHPH) on the obesity-related genes and cytokines, C57BL/6 mice were fed with high fat diet. C57BL/6 mice were divided into three groups and fed for 13weeks. Body weight change, diet intake change, final increase of body weight, the ratio of the adipocyte in body weight, the expression of leptin gene in primary adipocytes, the expression of UCP-2 in primary adipocytes, the production change of $TNF-\alpha$ and leptin in primary adipocytes, the expression of leptin in adipocytes tissue. The body weight of Mahwangpohang-tang(MHPH) intake mice was significantly lower than high fat diet group. The amount of the adipocyte in body weight was decreased Significantly. In primary adipocytes, leptin gene expression and the expression of UCP-2 did not change significantly. In primary adipocytes, the amount of $TNF-\alpha$ was significantly decreased at dose of $100{\mu}/ml$ density. In adipocytes tissue, the expression of leptin did not change significantly. These results suggest that MHPH may inhibit the expression of obesity-related genes and cytokines in high fat diet induced obesity mice

• 대한의생명과학회지
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• 제17권1호
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• pp.13-20
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• 2011

The peroxisome proliferator-activated receptor ${\alpha}$ ($PPAR{\alpha}$) is a nuclear transcription factor that plays a central role in lipid and lipoprotein metabolism. To investigate whether swim training improves obesity and lipid metabolism through $PPAR{\alpha}$ activation in female sham-operated (Sham) and ovariectomized (OVX) mice, we measured body weight, visceral adipose tissue mass, serum free fatty acid at 6 weeks as well as the expression of hepatic $PPAR{\alpha}$ target genes involved in fatty acid oxidation. Swim-trained mice had decreased body weight, visceral adipose tissue mass and serum free fatty acid levels compared to high fat diet fed control mice in both female Sham and OVX mice. These reductions were more prominent in OVX than in Sham mice. Swim training significantly increased hepatic mRNA levels of $PPAR{\alpha}$ target genes responsible for mitochondrial fatty acid ${\beta}$-oxidation, such as carnitine palmitoyltransgerase-1 (CPT-1), very long chain acyl-CoA dehydrogenase (VLCAD), and medium chain acyl-CoA dehydrogenase (MCAD) in OVX mice. However, swim trained female Sham mice did not increase hepatic mRNA levels of $PPAR{\alpha}$ target genes responsible for mitochondrial fatty acid ${\beta}$-oxidation compared to Sham control mice. These results indicate that swim training differentially regulates body weight and adipose tissue mass between OVX and Sham mice, at least in part due to differences in liver $PPAR{\alpha}$ activation.

• 대한융합한의학회지
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• 제5권2호
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• pp.23-27
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• 2023

Objectives: The purpose of this study was to investigate the ameliorative effects of the Epimedium koreanum Nakai (EK) on menopausal obesity in mice. Methods: To induce the menopausal obesity, female C57BL/6J mice were ovariectomized and fed with high fat diet for 12 weeks. 17β-estradiol was injected as a positive control and the extract of EK was orally administered 5 times per week for 6 weeks. Body weight, uterine weight and visceral fat weight were measured. The size of the adipocyte in visceral fat tissues was estimated by Hematoxylin and eosin staining. Fasting glucose level was estimated in serum. Results: Body weight and visceral fat weight were significantly decreased by EK treatment, while the uterine weight/body weight was increased in high fat diet-fed ovariectomized mice. The diameter of adipocyte in the visceral fat tissues was markedly reduced in EK-treated menopausal obese mice. In addition, the fasting blood glucose level was inhibited by oral EK administration. Conclusion: In conclusion, these results showed that EK has ameliorative effects on overweight after menopause. EK could be one of the alternative therapy for treating menopausal obesity.

• 대한의생명과학회지
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• 제24권4호
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• pp.380-389
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• 2018

Black vinegar has been traditionally used for supplemental flavoring on food, and commercialized beverages. Here, to investigate the effects on in vivo anti-obesity complications of black vinegar produced with herbal extracts, we evaluated on the biochemical effects of high-fat diet (HFD) induced mice compared to control fed ones. After a 84-day experiment HFD mice had higher (P < 0.05) weight gains, relative abdominal-fat pads, blood glucose level, serum/liver lipids, and serum nephron indices. Continuous oral treatment of three different concentration of herbal black vinegar (HBV; stock, 2-fold, and 4-fold diluted solution) to HFD mice showed that HBV reduced marked obesity (fat depositions, adipocyte hypertrophy), hyperglycemia, hyperlipidemia (serum total cholesterol, triglyceride, LDL-cholesterol levels), enhanced liver function (AST/ALT), and kidney function (BUN, creatine levels), respectively. Thus, HBV is expected to serve as an efficient and functional supplemental ingredients or food for the alleviation of obesity syndrome.

• Journal of Ginseng Research
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• 제46권3호
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• pp.454-463
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• 2022

Background: Gintonin-enriched fraction (GEF), a non-saponin fraction of ginseng, is a novel glycolipoprotein rich in hydrophobic amino acids. GEF has recently been shown to regulate lipid metabolism and browning in adipocytes; however, the mechanisms underlying its effects on energy metabolism and whether it affects sarcopenic obesity are unclear. We aimed to evaluate the effects of GEF on skeletal muscle atrophy in high-fat diet (HFD)-induced obese mice. Methods: To examine the effect of GEF on sarcopenic obesity, 4-week-old male ICR mice were used. The mice were divided into four groups: chow diet (CD), HFD, HFD supplemented with 50 mg/kg/day GEF, or 150 mg/kg/day GEF for 6 weeks. We analyzed body mass gain and grip strength, histological staining, western blot analysis, and immunofluorescence to quantify changes in sarcopenic obesity-related factors. Results: GEF inhibited body mass gain while HFD-fed mice gained 22.7 ± 2.0 g, whereas GEF-treated mice gained 14.3 ± 1.2 g for GEF50 and 11.8 ± 1.6 g for GEF150 by downregulating adipogenesis and inducing lipolysis and browning in white adipose tissue (WAT). GEF also enhanced mitochondrial biogenesis threefold in skeletal muscle. Furthermore, GEF-treated skeletal muscle exhibited decreased expression of muscle-specific atrophic genes, and promoted myogenic differentiation and increased muscle mass and strength in a dose-dependent manner (p < 0.05). Conclusion: These findings indicate that GEF may have potential uses in preventing sarcopenic obesity by promoting energy expenditure and attenuating skeletal muscle atrophy.

• The Korean journal of internal medicine
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• 제33권6호
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• pp.1210-1223
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• 2018

Background/Aims: The co-occurrence of obesity aggravates asthma symptoms. Diet-induced obesity increases helper T cell (TH) 17 cell differentiation in adipose tissue and the spleen. The 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor pravastatin can potentially be used to treat asthma in obese patients by inhibiting interleukin 17 (IL-17) expression. This study investigated the combined effects of pravastatin and anti-IL-17 antibody treatment on allergic inflammation in a mouse model of obesity-related asthma. Methods: High-fat diet (HFD)-induced obesity was induced in C57BL/6 mice with or without ovalbumin (OVA) sensitization and challenge. Mice were administered the anti-IL-17 antibody, pravastatin, or both, and pathophysiological and immunological responses were analyzed. Results: HFD exacerbated allergic airway inflammation in the bronchoalveolar lavage fluid of HFD-OVA mice as compared to OVA mice. Blockading of the IL-17 in the HFD-OVA mice decreased airway hyper-responsiveness (AHR) and airway inflammation compared to the HFD-OVA mice. Moreover, the administration of the anti-IL-17 antibody decreased the leptin/adiponectin ratio in the HFD-OVA but not the OVA mice. Co-administration of pravastatin and anti-IL-17 inhibited airway inflammation and AHR, decreased goblet cell numbers, and increased adipokine levels in obese asthmatic mice. Conclusions: These results suggest that the IL-17-leptin/adiponectin axis plays a key role in airway inflammation in obesity-related asthma. Our findings suggest a potential new treatment for IL-17 as a target that may benefit obesity-related asthma patients who respond poorly to typical asthma medications.

• Journal of Microbiology and Biotechnology
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• 제33권1호
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• pp.96-105
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• 2023

Probiotic supplements have promising therapeutic effects on chronic diseases. In this study, we demonstrated the anti-obesity effects of two potential probiotics, Bifidobacterium bifidum DS0908 (DS0908) and Bifidobacterium longum DS0950 (DS0950). Treatment with DS0908 and DS0950 postbiotics significantly induced the expression of the brown adipocyte-specific markers UCP1, PPARγ, PGC1α, PRDM16 and beige adipocyte-specific markers CD137, FGF21, P2RX5, and COX2 in C3H10T1/2 mesenchymal stem cells (MSCs). In mice with high-fat diet (HFD)-induced obesity, both potential probiotics and postbiotics noticeably reduced body weight and epididymal fat accumulation without affecting food intake. DS0908 and DS0950 also improved insulin sensitivity and glucose use in mice with HFD-induced obesity. In addition, DS0908 and DS0950 improved the plasma lipid profile, proved by reduced triglyceride, low-density lipoprotein, and cholesterol levels. Furthermore, DS0908 and DS0950 improved mitochondrial respiratory function, confirmed by the high expression of oxidative phosphorylation proteins, during thermogenesis induction in the visceral and epididymal fat in mice with HFD-induced obesity. Notably, the physiological and metabolic changes were more significant after treatment with potential probiotic culture-supernatants than those with the bacterial pellet. Finally, gene knockdown and co-treatment with inhibitor-mediated mechanistic analyses showed that both DS0908 and DS0950 exerted anti-obesity-related effects via the PKA/p38 MAPK signaling activation in C3H10T1/2 MSCs. Our observations suggest that DS0908 and DS0950 could potentially alleviate obesity as dietary supplements.

• 한방비만학회지
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• 제21권2호
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• pp.49-58
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• 2021

Objectives: The purpose of this study was to investigate the effect of white pan bread added with Kamut (Triticum turgidum spp.) on high fat diet (HFD)-induced obese C57BL/6 mice. Methods: The white pan bread or white pan bread with Kamut (BK) were administered for 8 weeks in HFD-induced obese C57BL/6 mice. To evaluate the effect and its mechanisms of BK on obese mice, we measured body weight change, serum lipid profiles, histopathological analysis, and protein expression of CCAAT/enhancer binding protein-α (C/EBPα) in the liver. Results: Administration of BK significantly decreased body weight in HFD-induced obese mice. In addition, BK-administered group significantly reduced serum total cholesterol, glucose, and high-density lipoprotein cholesterol levels compared with the HFD-induced control group. The HFD-induced mice had damaged liver tissue and increased the size of adipose tissue, but BK-administered group attenuated liver damage and decreased the size of adipocyte. Furthermore, administration of BK significantly down-regulated C/EBPα in the liver compared with HFD-fed mice. In particular, BK-administered group has higher inhibited body weight, serum lipid profiles, and C/EBPα expressions than white pan bread-administered group. Conclusions: This study demonstrated that administration of BK attenuated HFD-induced obesity by regulation of C/EBPα than consumption of white pan bread. Therefore, BK could be developed as a bread for prevention of obesity.