• Biomedical Science Letters
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• v.24 no.4
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• pp.311-318
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• 2018

Vitamin C (ascorbic acid) supplementation has been suggested to negatively correlate with obesity in humans and other animals. Previous studies, including ours, have demonstrated that a high-fat diet (HFD) induces obesity and related diseases such as hyperlipidemia, hyperglycemia, insulin resistance, and nonalcoholic fatty liver disease. Here, we investigated the effects of vitamin C on visceral adipocyte hypertrophy and glucose intolerance in C57BL/6J mice. Mice received a low-fat diet (LFD, 10% kcal fat), HFD (45% kcal fat), or the same HFD supplemented with vitamin C (HFD-VC, 1% w/w) for 15 weeks. Visceral adiposity and glucose intolerance were examined using metabolic measurements, histology, and gene expression analyses. Mice in the HFD-VC supplementation group had reduced body weight, mesenteric fat mass, and mesenteric adipocyte size compared with HFD-fed mice. Vitamin C intake in obese mice also decreased the mRNA levels of lipogenesis-related genes (i.e., stearoyl-CoA desaturase 1 and sterol regulatory element-binding protein 1c) in mesenteric adipose tissues, inhibited hyperglycemia, and improved glucose tolerance. In addition, vitamin C attenuated the HFD-induced increase in the size of pancreatic islets. These results suggest that vitamin C suppresses HFD-induced visceral adipocyte hypertrophy and glucose intolerance in part by decreasing the visceral adipose expression of genes involved in lipogenesis.

• Journal of Microbiology and Biotechnology
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• v.31 no.11
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• pp.1568-1575
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• 2021

Obesity and related metabolic diseases are major problems worldwide. Some probiotics are currently considered potential therapeutic strategies for obesity. We aimed to investigate the anti-obesity efficacy of Latilactobacillus sakei WIKIM31 in obese mice induced by a high fat diet. The administration of a high-fat diet with L. sakei WIKIM31 reduced body weight gain, epididymal fat mass, triglyceride and total cholesterol levels in the blood, and remarkably decreased the expression of lipogenesis-related genes in the epididymal adipose tissue and liver. Interestingly, intake of L. sakei WIKIM31 improved gut barrier function by increasing the gene expression of tight junction proteins and suppressing the inflammatory responses. Additionally, L. sakei WIKIM31 enhanced the production of short-chain fatty acids, such as butyrate and propionate, in the intestinal tract. These results showed that L. sakei WIKIM31 can be used as a potential therapeutic probiotic for obesity.

• Journal of the Korean Applied Science and Technology
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• v.38 no.2
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• pp.356-367
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• 2021

This study investigated the effect of swimming exercise on inflammation in non-alcoholic fatty liver using animal models of postmenopausal obese women. Experimental animals were divided into a sham-operate + non-swimming trained group (S/N), an ovariectomize + non-swimming trained group (O/N) and an ovariectomize + swimming trained group (O/S), and were bred while eating a high fat diet for 8 weeks. Fat accumulation in liver tissue, liver weight, and serum AST and ALT increased in O/N compared to S/N, but decreased in O/S compared to O/N. Compared to S/N, O/N decreased the gene expression of IκBα in liver tissue and increased gene expression of MCP-1, IL-6, and TNF-α. But compared to O/N, O/S increased the gene expression of IκBα in liver tissue and decreased gene expression of MCP-1, IL-6, and TNF-α. In conclusion, this study suggested that swimming exercise was effective in improving physical health by improving inflammation in non-alcoholic fatty liver in obese mice induced obesity by high fat diet after ovariectomy.

• The Journal of Internal Korean Medicine
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• v.35 no.2
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• pp.195-207
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• 2014

Objectives : The purpose of this study was to investigate how Rhei Radix et Rhizoma affects on insulin resistance and adipose tissue inflammatory response in high fat diet induced obese C57BL/6 mice. Methods : Obesity was induced in C57BL/6 mice by high fat diet for 12 weeks. Models were divided into 3 groups (n=6) of normal diet, high fat diet (HFD), and high fat diet with Rhei Radix et Rhizoma and investigated for 12 weeks. We measured body weight, FBS and oral glucose tolerance test (OGTT), serum insulin, homeostatic model assessment-insulin resistance (HOMA-IR), weight of liver and epididymal fat pad. Inflammatory markers such as adipose tissue macrophage (ATM), tumor necrosis factor-${\alpha}$ and interlukin-10 and CD68 of epididymal adipocyte were determined to evaluate the effect of Rhei Radix et Rhizoma on adipose tissue inflammation. Results : Compared with the HFD group, we observed loss of body weight and epididymal fat pad weight, improvement of glucose level and HOMA-IR, reduction of ATM and gene expression of TNF-${\alpha}$, CD68 in the high fat diet with Rhei Radix et Rhizoma group. Conclusions : This study suggests that Rhei Radix et Rhizoma has effects on insulin resistance and adipose tissue inflammatory response in high fat diet induced obese mice.

• Preventive Nutrition and Food Science
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• v.16 no.3
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• pp.210-216
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• 2011

Capsaicin is a pungent component of red pepper, which is widely consumed as food adjuncts. The present study was performed to investigate anti-obesity effects of capsaicin in diet-induced obese rats. Male Sprague-Dawley rats (n=14) were fed with a high-fat diet (Control) or high-fat diet containing 0.016% capsaicin (w/w) (Capsaicin) for 8 weeks. The final body weight and the mass of white adipose tissue were significantly lower in capsaicin supplemented group compared to control. Dietary capsaicin ameliorated lipid profiles with decrease in the plasma concentrations of triglycerides and total cholesterol, and decrease in the levels of total lipids and triglycerides in the liver. Activity of glycerol-3-phosphate dehydrogenase (GPDH), an indicator of triglyceride biosynthesis in white adipose tissue, decreased by 35% in the group supplemented with capsaicin. However, consumption of capsaicin increased the expression of uncoupling protein 2 (UCP2) in white adipose tissue, which is related to energy consumption. Our data suggests that capsaicin may reduce body weight and fat accumulation in high fat diet-induced obese rats. These effects may be mediated, at least partially, by the upregulation of UCP2 gene expression and its ability to inhibit GPDH activity.

• Journal of Ginseng Research
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• v.41 no.1
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• pp.52-59
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• 2017

Background: Korean Red Ginseng extract (KRG, Panax ginseng Meyer) and its constituents have been used for treating diabetes. However, in diet-induced obese mice, it is unclear whether KRG can enhance the glucose-lowering action of rosiglitazone (ROSI), a peroxisome proliferator-activated receptor gamma synthetic activator. Methods: Oral glucose tolerance tests (oGTTs) were performed after 4 days of treatment with a vehicle (CON), KRG [500 mg/kg body weight (b.w.)], ROSI (3.75 mg/kg b.w, 7.5 mg/kg b.w, and 15 mg/kg b.w.), or ROSI and KRG (RK) in obese mice on a high-fat diet. Adipose tissue morphology, crown-like structures (CLSs), and inflammation were compared by hematoxylin-eosin staining or quantitative reverse transcription polymerase chain reaction. Results: The area under the glucose curve (AUC) was significantly lower in the RK group (15 mg/kg b.w. and 500 mg/kg b.w. for ROSI and KRG, respectively) than in the CON group. There was no significant difference in the AUC between the CON and the other groups. Furthermore, the AUC was significantly lower in the RK group than in the ROSI group. The expression of the Ccl2 gene and the number of CLSs were significantly reduced in the RK group than in the CON group. Conclusion: Our results show a potential enhancement of ROSI-induced improvement of glucose regulation by the combined treatment with KRG.

• IMMUNE NETWORK
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• v.16 no.3
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• pp.189-194
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• 2016

Obesity is characterized as an accumulation of adipose tissue mass represented by chronic, low-grade inflammation. Obesity-derived inflammation involves chemokines as important regulators contributing to the pathophysiology of obesity-related diseases such as cardiovascular disease, diabetes and some cancers. The obesity-driven chemokine network is poorly understood. Here, we identified the profiles of chemokine signature between human preadipocytes and adipocytes, using PCR arrays and qRT-PCR. Both preadipocytes and adipocytes showed absent or low levels in chemokine receptors in spite of some changes. On the other hand, the chemokine levels of CCL2, CCL7-8, CCL11, CXCL1-3, CXCL6 and CXCL10-11 were dominantly expressed in preadipocytes compared to adipocytes. Interestingly, CXCL14 was the most dominant chemokine expressed in adipocytes compared to preadipocytes. Moreover, there is significantly higher protein level of CXCL14 in conditioned media from adipocytes. In addition, we analyzed the data of the chemokine signatures in adipocytes obtained from healthy lean and obese postmenopausal women based on Gene Expression Omnibus (GEO) dataset. Adipocytes from obese individuals had significantly higher levels in chemokine signature as follows: CCL2, CCL13, CCL18-19, CCL23, CCL26, CXCL1, CXCL3 and CXCL14, as compared to those from lean ones. Also, among the chemokine networks, CXCL14 appeared to be the highest levels in adipocytes from both lean and obese women. Taken together, these results identify CXCL14 as an important chemokine induced during adipogenesis, requiring further research elucidating its potential therapeutic benefits in obesity.

• Journal of Life Science
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• v.27 no.12
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• pp.1462-1469
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• 2017

The purpose of this study was to investigate the effects of resveratrol supplementation on inflammasome, inflammation, and macrophage markers in subcutaneous adipose tissue of high-fat-diet-induced obese mice. C57BL/6 mice were randomly assigned to three groups: normal diet control (NC; n=10), high-fat diet control (HC; n=10), or high fat with resveratrol (HRE; n=10) group. The mice were fed a high-fat diet (60% of calories from fat) or normal diet (18% of calories from fat). Resveratrol dissolved in a 0.1ml solution of dimethyl sulfoxide was supplemented orally at 25 mg/kg body weight. After 15 weeks, the body weight was significantly higher in the high-fat diet group than in the normal diet group. The inflammasome markers NLRP3, ASC, and caspase1 were significantly lower in the HRE group than in the HC group. The levels of an inflammation marker, IL-18, were also significantly lower in the HRE group than in the NC and HC groups. The levels of macrophage markers F480 and CD86 were significantly lower in the HRE group than in the HC group. The levels of the M2 macrophage marker CD206 were significantly decreased in the HC and HRE groups. Resveratrol had a positive effect on ameliorating the complications of high fat diet-induced obesity by reducing inflammasome and M1 macrophage gene expressions. However, resveratrol supplementation did not reduce inflammation gene expression.

• Nutritional Sciences
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• v.6 no.2
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• pp.73-77
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• 2003

PAI-1 (plasminogen activator inhibitor-1), leptin, and resistin are synthesized and secreted by Int cells of rodents and have recently been postulated to be an important link to obesity. This study was conducted to identify the nutritional regulation of PAI-1, leptin, and resistin gene expression in 0b/ob mice. The mice were divided into four groups according to nutritional status: control, 48 hour fasting, 48 hour-fasting/12 hour-refeeding, and 48 hour-fasting/24 hour-refeeding. The mRNA levels of each peptide were measured by semi-quantitative RT-PCR. In visceral fat tissue, the level of PAI-1 mRNA increased markedly when 48h-fasted animals were refed with a high carbohydrate-low fat diet. However, lasting/refeeding did not appreciably change PAI-1 mRNA levels in subcutaneous fat tissue. Similar results were obtained for resistin mRNA levels in both types of fat tissues. These findings suggest that visceral adipose tissue might be more sensitively involved in the nutritional regulation of PAI-1 and resistin gene expression compared to subcutaneous fat tissue. The level of leptin mRNA decreased markedly in the 48h-fasted animals, and increased markedly when 48h-fasted animals were refed with a high carbohydrate-low fat diet. The nutritional regulation of leptin mRNA showed similar patterns in both types of fat tissues. In conclusion, the nutritional regulation of gene expression encoding PAI-1, resistin, and leptin from adipocytes may vary according to the type of adipose tissue.

• Asian-Australasian Journal of Animal Sciences
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• v.15 no.7
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• pp.932-937
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• 2002

A partial genome scan using porcine microsatellites was carried out to detect quantitative trait loci (QTL) for backfat thickness (BFT) in a pig reference population. This population carried QTL on chromosomes 1, 13 and 18. The QTL on chromosome 1 was located between marker loci S0113 and SW1301. The QTL corresponded to very low density lipoprotein receptor gene (VLDLR) in location and in biological effects, suggesting that VLDLR might be a candidate gene. The QTL found on chromosome 13 was found between marker loci SWR1941 and SW864, but significance for the marker-trait association was inconsistent by using data with different generations. The QTL on chromosome 18 was discovered between markers S0062 and S0117, and it was in proximity of the regions where IGFBP3 and GHRHR were located. The porcine obese gene might be also a candidate gene for the QTL on chromosome 18. In order to understand genetic architecture of BFT better, fine mapping and positional comparative candidate gene analyses are necessary.