• Title/Summary/Keyword: Adipokine

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Circulating Levels of Adipokines Predict the Occurrence of Acute Graft-versus-host Disease

  • Kim, Jin Sook;You, Da-Bin;Lim, Ji-Young;Lee, Sung-Eun;Kim, Yoo-Jin;Kim, Hee-Je;Chung, Nack-Gyun;Min, Chang-Ki
    • IMMUNE NETWORK
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    • v.15 no.2
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    • pp.66-72
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    • 2015
  • Currently, detecting biochemical differences before and after allogeneic stem cell transplantation (SCT) for improved prediction of acute graft-versus-host disease (aGVHD) is a major clinical challenge. In this pilot study, we analyzed the kinetics of circulating adipokine levels in patients with or without aGVHD before and after allogeneic SCT. Serum samples were obtained and stored at $-80^{\circ}C$ within 3 hours after collection, prior to conditioning and at engraftment after transplantation. A protein array system was used to measure the levels of 7 adipokines of patients with aGVHD (n=20) and without aGVHD (n=20). The resistin level at engraftment was significantly increased (p<0.001) after transplantation, regardless of aGVHD occurrence. In the non-aGVHD group, the concentrations of the hepatocyte growth factor (HGF) (mean values${\pm}$SD; $206.6{\pm}34.3$ vs. $432.3{\pm}108.9pg/ml$, p=0.040) and angiopoietin-2 (ANG-2) (mean values${\pm}$SD; $3,197.2{\pm}328.3$ vs. $4,471.8{\pm}568.4pg/ml$, p=0.037) at engraftment were significantly higher than those of the pre-transplant period, whereas in the aGVHD group, the levels of adipokines did not change after transplantation. Our study suggests that changes in serum HGF and ANG-2 levels could be considered helpful markers for the subsequent occurrence of aGVHD.

Cloning of porcine chemerin, ChemR23 and GPR1 and their involvement in regulation of lipogenesis

  • Huang, Jianfeng;Zhang, Jian;Lei, Ting;Chen, Xiaodong;Zhang, Yan;Zhou, Lulu;Yu, An;Chen, Zhilong;Zhou, Ronghua;Yang, Zaiqing
    • BMB Reports
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    • v.43 no.7
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    • pp.491-498
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    • 2010
  • Chemerin is a novel adipokine which is abundant in adipose tissue to promote adipocyte differentiation and with significant relativity to BMI and insulin sensitivity. We report here the molecular characterization of porcine chemerin and its receptors ChemR23 and GPR1, as well as their transcriptional regulation during lipogenesis. Chemerin was mainly expressed in liver, intestine, kidney and adipose tissue, consistent with the expression pattern of GPR1, but not ChemR23, which was predominantly present in spleen and temperately in adipose tissue. We further investigated the lipogenesis-related transcriptional activation of $PPAR{\gamma}$ and KLF15 on chemerin and its receptors. The data showed that KLF15, but not $PPAR{\gamma}$, can up-regulate the mRNA level of chemerin, ChemR23 and GPR1, which was consistent with the results of luciferase assay that confirmed the effect of KLF15 on ChemR23 promoter. Taken together, our data provide basic molecular information for the further investigation on the function of chemerin in lipogenesis.

Anti-Obesity Effect of Krill Oil by Regulation of Adipokines in High Fat Diet-Induced Mouse Model (고지방식이 동물모델에서 크릴오일의 아디포카인 조절을 통한 항비만 효과)

  • Kim, Ji Hyun;He, Mei Tong;Seo, Hyo Jeong;Lee, Dongjun;Cho, Eun Ju
    • Journal of the Korea Academia-Industrial cooperation Society
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    • v.21 no.11
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    • pp.201-208
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    • 2020
  • This study examined the anti-obesity effect of krill oil (KO) by regulating adipokines in a high-fat diet (HFD)-induced obese mouse model. The mice were fed a 60 kcal% HFD for 16 weeks, and KO was then administered at an oral dose of 100, 200, and 500 mg/kg/day for four weeks before the end of the experiment. The administration of KO at concentrations of 200 and 500 mg/kg/day decreased body weight gain significantly compared with the HFD-fed control group. In addition, the HFD-fed control group showed the abnormal release of adipokines by an increase in leptin and decrease in adiponectin, compared to the normal diet-fed normal group. On the other hand, KO (500 mg/kg/day)-administered group attenuated the abnormal release of adipokines by the down-regulation of leptin and the up-regulation of adiponectin. Therefore, KO could be a promising therapeutic agent for obesity by the regulation of adipokines.

Single Nucleotide Polymorphism in the Coding Region of Bovine Chemerin Gene and Their Associations with Carcass Traits in Japanese Black Cattle

Anti-Obesity Effect of Ethyl Acetate Extracts from Agrimonia pilosa Ledeb. in 3T3-L1 Preadipocytes (3T3-L1 지방전구세포에서 용아초 에틸아세테이트 추출물의 항비만 효과)

  • Lee, Jung-A;Ahn, Eun-Kyung;Hong, Seong-Su;Oh, Joa-Sub
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.41 no.2
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    • pp.161-167
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    • 2012
  • To evaluate the anti-obesity effect of Agrimonia pilosa L., this study investigated that ethyl acetate extract from A. pilosa L. (EAAP) suppresses lipid accumulation and inhibits expression of adipogenic marker genes, such as peroxisome proliferator activated receptor ${\gamma}$ (PPAR${\gamma}$), CCAAT-enhancer-binding protein ${\alpha}$ (C/EBP${\alpha}$), glucose transporter 4 (GLUT4), and adiponectin in 3T3-L1 preadipocytes. We demonstrated that EAAP inhibited adipocyte differentiation and expression of PPAR${\gamma}$ and C/EBP${\alpha}$ mRNA levels in a dose-dependent manner. In addition, EAAP reduced the PPAR${\gamma}$ transcriptional activity stimulated by rosiglitazone in HEK 293T cells and decreased the expression of GLUT4 and adiponectin in 3T3-L1 cells. These results suggest that EAAP inhibits preadipocyte differentiation and adipogenesis by blocking of PPAR${\gamma}$ and C/EBP${\alpha}$ gene expression in 3T3-L1 cells.

Effects of a Caragana sinica Water Extract on Lipid and Glucose Metabolism in Ovariectomized Rats (골담초 열수 추출물의 갱년기 이후 지질 및 당질 대사 개선 효능)

  • Lee, Sang Chul;Chung, Soo Im;Kang, Mi Young
    • Korean Journal of Plant Resources
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    • v.29 no.5
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    • pp.532-538
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    • 2016
  • Menopause is characterized by a decrease in estrogen production by the ovaries. Furthermore, the risk of developing chronic diseases including cardiovascular disease, obesity, and diabetes increases in menopausal women. In this study, we evaluated the ability of Caragana sinica (CS) to affect lipid and glucose metabolism in an ovariectomized Sprague-Dawley rat model of induced menopause. The animals were divwided randomly into three groups: sham-operated rats (SHAM), ovariectomized rats (OVX), and ovariectomized rats treated with 1% water extract of CS (OVX-CS). The OVX-CS treated mice showed a significant decrease in body weight, adipose tissue, triglyceride, and total cholesterol. Improved lipid and glucose profiles were also observed, and were attributed to suppression of hepatic lipogenesis and adipokine production and regulation of glucose-regulating enzyme activity. Therefore, these findings indicate a potential use for CS as a functional food for menopause-induced hyperlipidemia and hyperglycemia.

Osteoarthritis of the Temporomandibular Joint (측두하악관절의 골관절염)

  • Lee, Jeong-Yun
    • Journal of Oral Medicine and Pain
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    • v.38 no.1
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    • pp.87-95
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    • 2013
  • Osteoarthritis (OA) of the temporomandibular joint (TMJ) is a severe form of temporomandibular disorders (TMDs), presenting gradual breakdown of articular cartilage and subchondral bone by the functional load sustained to exceed the physiologic tolerance of the joint. In such a joint loaded, offensive bioactive materials such as matrix degrading proteins, cytokines, and free radicals increase in concentration to shift the tissue response in the joint to degeneration from regeneration or remodeling. Recently, it has been issued that obesity can play an offensive role in pathogenesis of OA in a metabolic way. Adipokines released by adipose cells are present at higher concentration in the arthritic joint and joints of obese individuals. However, because of conflicting data reported, further scientific study should be performed to elucidate the practical role of adipokines in pathogenesis of TMJ OA. As far as the clinical signs and symptoms of TMJ OA are not much different from those of other forms of TMD and any definitive treatment modality to control directly the bone resorptive activity is not available yet, the treatment of TMJ OA should be directed to reduce the physical load and enhance the physiologic tolerance of the joint by means of conservative treatment such as physical therapy, medication, and occlusal splint therapy for sufficient period and, if needed after that, supplementary surgical procedure such as intra-articular injection, arthrocenthesis, and arthroscopic surgery that have turned out to be effective to control OA signs and symtpoms. Enthusiastic reassurance and motivation for patients to control behaviors for themselves to reduce unnecessary functional load in daily life is very important for the joint to reach to more favorable orthopedic stability of the TMJ more quickly, guaranteeing more successful management TMJ OA.

Effects of luteolin on chemical induced colon carcinogenesis in high fat diet-fed obese mouse (고지방식이를 급여한 비만 마우스에서 luteolin이 화학적으로 유도한 대장암 발생에 미치는 영향)

  • Park, Jeong-Eun;Kim, Eunjung
    • Journal of Nutrition and Health
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    • v.51 no.1
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    • pp.14-22
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    • 2018
  • Purpose: Colorectal cancer, which is one of the most commonly diagnosed cancers in developing and developed countries, is highly associated with obesity. The association is largely attributed to changes to western style diets in those countries containing high-fat and high-energy. Luteolin (LUT) is a known potent inhibitor of inflammation, obesity, and cancer. In this study, we investigated the effects of LUT on chemical-induced colon carcinogenesis in high fat diet (HFD)-fed obese mice. Methods: Five-week-old male C57BL/6 mice received a single intraperitoneal injection of azoxymethane (AOM) at a dose of 12.5 mg/kg body weight. Mice were then divided into four groups (n = 10) that received one of the following diets for 11 weeks after the AOM injection: normal diet (ND); HFD; HFD with 0.0025% LUT (HFD LL); HFD with 0.005% LUT (HFD HL). One week after AOM injection, animals received 1~2% dextran sodium sulfate in their drinking water over three cycles consisting of five consecutive days each that were separated by 16 days. Results: Body weight, ratio of colon weight/length, and tumor multiplicity increased significantly in the HFD group compared to the ND group. Luteolin supplementation of the HFD significantly reduced the ratio of colon weight/length and colon tumors, but not body weight. The levels of plasma $TNF-{\alpha}$ and colonic expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 protein increased in response to HFD, but were suppressed by LUT supplementation. Immunohistochemistry analysis also showed that iNOS expression was decreased by LUT. Conclusion: Consumption of LUT may reduce the risk of obesity-associated colorectal cancer by suppression of colonic inflammation.

Effect of the anti-IL-17 antibody on allergic inflammation in an obesity-related asthma model

  • Liang, Lin;Hur, Jung;Kang, Ji Young;Rhee, Chin Kook;Kim, Young Kyoon;Lee, Sook Young
    • The Korean journal of internal medicine
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    • v.33 no.6
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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.

Effects of caloric restriction on the expression of lipocalin-2 and its receptor in the brown adipose tissue of high-fat diet-fed mice

  • Park, Kyung-Ah;Jin, Zhen;An, Hyeong Seok;Lee, Jong Youl;Jeong, Eun Ae;Choi, Eun Bee;Kim, Kyung Eun;Shin, Hyun Joo;Lee, Jung Eun;Roh, Gu Seob
    • The Korean Journal of Physiology and Pharmacology
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    • v.23 no.5
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    • pp.335-344
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    • 2019
  • Obesity causes inflammation and impairs thermogenic functions in brown adipose tissue (BAT). The adipokine lipocalin 2 (LCN2) has been implicated in inflammation and obesity. Herein, we investigated the protective effects of caloric restriction (CR) on LCN2-mediated inflammation and oxidative stress in the BAT of high-fat diet (HFD)-fed mice. Mice were fed a HFD for 20 weeks and then either continued on the HFD or subjected to CR for the next 12 weeks. CR led to the browning of the white fat-like phenotype in HFD-fed mice. Increased expressions of LCN2 and its receptor in the BAT of HFD-fed mice were significantly attenuated by CR. Additionally, HFD+CR-fed mice had fewer neutrophils and macrophages expressing LCN2 and iron-positive cells than HFD-fed mice. Further, oxidative stress and mitochondrial fission induced by a HFD were also significantly attenuated by CR. Our findings indicate that the protective effects of CR on inflammation and oxidative stress in the BAT of obese mice may be associated with regulation of LCN2.