• 제목/요약/키워드: obese gene

검색결과 153건 처리시간 0.028초

Vitamin C Inhibits Visceral Adipocyte Hypertrophy and Lowers Blood Glucose Levels in High-Fat-Diet-Induced Obese C57BL/6J Mice

  • Park, Younghyun;Jang, Joonseong;Lee, Dongju;Yoon, Michung
    • 대한의생명과학회지
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    • 제24권4호
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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.

Latilactobacillus sakei WIKIM31 Decelerates Weight Gain in High-Fat Diet-Induced Obese Mice by Modulating Lipid Metabolism and Suppressing Inflammation

  • Park, Sung-Soo;Lim, Seul Ki;Lee, Jieun;Park, Hyo Kyeong;Kwon, Min-Sung;Yun, Misun;Kim, Namhee;Oh, Young Joon;Choi, Hak-Jong
    • Journal of Microbiology and Biotechnology
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    • 제31권11호
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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.

비알코올성 지방간을 가진 난소절제 쥐에서 염증에 대한 수영운동의 영향 (The effect of swimming exercise on inflammation in ovariectomized mice with non-alcoholic fatty liver)

  • 정선효
    • 한국응용과학기술학회지
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    • 제38권2호
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    • pp.356-367
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    • 2021
  • 본 연구는 폐경 후 비만 여성의 동물모델을 이용하여 수영운동이 비알코올성 지방간에서 염증에 미치는 영향을 조사하였다. 실험동물은 수영운동을 하지 않은 모의수술군(S/N), 수영운동을 하지 않은 난소절제 수술군(O/N) 및 수영운동을 실시한 난소절제 수술군(O/S)으로 구분되어 8주 동안 고지방식이 사료를 섭취하면서 사육되었다. 간 조직의 지방축적, 간 무게 및 혈청 속 AST와 ALT는 S/N에 비해 O/N에서 증가하였으나, O/N에 비해 O/S에서는 감소하였다. S/N에 비해 O/N는 간 조직에서의 IκBα의 유전자 발현이 감소하였고 MCP-1, IL-6 및 TNF-α의 유전자 발현은 증가하였다. 그러나 O/N에 비해 O/S는 간 조직에서의 IκBα이 증가하였고 MCP-1, IL-6 및 TNF-α의 유전자 발현은 감소하였다. 결론적으로 본 연구는 난소절제 후 고지방식이의 섭취로 비만이 유도된 비만 쥐에서 수영운동이 비만으로 유도된 비알코올성 지방간에서 염증을 개선함으로써 건강증진에 효과적임을 제시하였다.

대황(大黃)이 고지방식이로 비만이 유발된 C57BL/6 mouse의 지방조직 염증 및 인슐린 저항성에 미치는 영향 (Effects of Rhei Radix et Rhizoma on Insulin Resistance and Adipose Tissue Inflammatory Response in High Fat Diet Induced Obese C57BL/6 Mice)

  • 최승범;마영훈;한양희;정수정;조홍석
    • 대한한방내과학회지
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    • 제35권2호
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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.

Reduction of Body Weight by Capsaicin is Associated with Inhibition of Glycerol-3-Phosphate Dehydrogenase Activity and Stimulation of Uncoupling Protein 2 mRNA Expression in Diet-induced Obese Rats

  • Ann, Ji-Young;Lee, Mak-Soon;Joo, Hyun-Jin;Kim, Chong-Tai;Kim, Yang-Ha
    • Preventive Nutrition and Food Science
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    • 제16권3호
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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.

The effect of Korean Red Ginseng extract on rosiglitazone-induced improvement of glucose regulation in diet-induced obese mice

  • Oh, Mi-Jeong;Kim, Hyun-Ju;Park, Eun-Young;Ha, Na-Hee;Song, Mun-Gyu;Choi, Sang-Hyun;Chun, Boe-Gwun;Kim, Dong-Hoon
    • Journal of Ginseng Research
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    • 제41권1호
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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.

Differential Chemokine Signature between Human Preadipocytes and Adipocytes

  • Rosa Mistica C. Ignacio;Carla R. Gibbs;Eun-Sook Lee;Deok-Soo Son
    • IMMUNE NETWORK
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    • 제16권3호
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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.

라스베라트롤 투여가 고지방식이 비만쥐의 지방조직에서의 inflammasome과 대식세포 마커에 미치는 영향 (Resveratrol Ameliorates High-fat-induced Metabolic Complications by Changing the Expression of Inflammasome Markers and Macrophage M1 and M2 Markers in Obese Mice)

  • 이영란;피핏 피트리아니;박희근;이왕록
    • 생명과학회지
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    • 제27권12호
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    • pp.1462-1469
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    • 2017
  • 본 연구 목적은 고지방식이 유도 비만 쥐의 피하지방조직에서 라스베라트롤 투여가 대식세포 침윤관련 염증인자에 미치는 영향을 규명하고자 하였다. 본 연구를 위해 정상식이군, 고지방식이군, 고지방식이+라스베라트롤 투여군으로 분류한 후, 라스베라트롤 투여군은 15주간 25 mg/kg 농도로 Dimethyl Sulfoxide에 용해하여 투여하였으며, 비교군은 Dimethyl Sulfoxide 용액만을 투여하였다. 연구결과 고지방식이군은 정상식이군에 비하여 체중이 유의하게 증가하였고, 라스베라트롤 투여군에서 고지방식이 군보다 NLRP3. ASC, Casepase1 mRNA 발현이 감소하였다. 또한 염증마커로 알려진 IL-18 mRNA 발현이 라스베라트롤 투여군에서 정상식이군과 고지방식이군보다 낮게 나타났다. 대식세포 침윤 마커인 F480, CD86 mRNA 발현에서도 라스베라트롤 투여군에서 고지방식이 군보다 유의한 감소를 보였다. 따라서 라스베라트롤 투여는 고지방식이 유도 비만 상황에서 대식세포 침윤 염증과 inflammasome에 긍정적인 영향을 미치는 것으로 보여진다.

Nutritional Regulation of Plasminogen Activator Inhibitor-1, Leptin and Resistin Gene Expression in Obese Mouse

  • Lee, Hyun-Jung;Yang, Jeong-Lye;Kim, Young-Hwa;Kim, Yangha
    • Nutritional Sciences
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    • 제6권2호
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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.

Quantitative Trait Loci Mapping for Porcine Backfat Thickness

  • Wu, X.L.;Lee, C.;Jiang, J.;Peng, Y.L.;Yan, H.F.;Yang, S.L.;Xiao, B.N.;Liu, X.C.;Shi, Q.S.
    • Asian-Australasian Journal of Animal Sciences
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    • 제15권7호
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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.