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Effect of Green Tea Extract/Poly-γ-Glutamic Acid Complex in Obese Type 2 Diabetic Mice
Ki-Cheor Bae, Jae-Hyung Park, Ann-Yae Na, Sun-Joo Kim, Shinbyoung Ahn, Sang-Pyo Kim, Byung-Chul Oh, Ho-Chan Cho, Yong Woon Kim, Dae-Kyu Song
Diabetes Metab J. 2013;37(3):196-206.   Published online June 14, 2013
DOI: https://doi.org/10.4093/dmj.2013.37.3.196
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  • 44 Download
  • 10 Crossref
AbstractAbstract PDFPubReader   
Background

The increasing prevalence of type 2 diabetes mellitus (T2DM) is associated with the rapid spread of obesity. Obesity induces insulin resistance, resulting in β-cell dysfunction and thus T2DM. Green tea extract (GTE) has been known to prevent obesity and T2DM, but this effect is still being debated. Our previous results suggested that circulating green tea gallated catechins (GCs) hinders postprandial blood glucose lowering, regardless of reducing glucose and cholesterol absorption when GCs are present in the intestinal lumen. This study aimed to compare the effect of GTE with that of GTE coadministered with poly-γ-glutamic acid (γ-PGA), which is likely to inhibit the intestinal absorption of GCs.

Methods

The db/db mice and age-matched nondiabetic mice were provided with normal chow diet containing GTE (1%), γ-PGA (0.1%), or GTE+γ-PGA (1%:0.1%) for 4 weeks.

Results

In nondiabetic mice, none of the drugs showed any effects after 4 weeks. In db/db mice, however, weight gain and body fat gain were significantly reduced in the GTE+γ-PGA group compared to nondrug-treated db/db control mice without the corresponding changes in food intake and appetite. Glucose intolerance was also ameliorated in the GTE+γ-PGA group. Histopathological analyses showed that GTE+γ-PGA-treated db/db mice had a significantly reduced incidence of fatty liver and decreased pancreatic islet size. Neither GTE nor γ-PGA treatment showed any significant results.

Conclusion

These results suggest that GTE+γ-PGA treatment than GTE or γ-PGA alone may be a useful tool for preventing both obesity and obesity-induced T2DM.

Citations

Citations to this article as recorded by  
  • Preparation of Type-A Gelatin/Poly-γ-Glutamic Acid Nanoparticles for Enhancing the Stability and Bioavailability of (-)-Epigallocatechin Gallate
    Weijie Zhang, Huangchen Shen, Ying Li, Kai Yang, Peng Lei, Yian Gu, Liang Sun, Hong Xu, Rui Wang
    Foods.2023; 12(9): 1748.     CrossRef
  • γ-PGA-Rich Chungkookjang, Short-Term Fermented Soybeans: Prevents Memory Impairment by Modulating Brain Insulin Sensitivity, Neuro-Inflammation, and the Gut–Microbiome–Brain Axis
    Do-Youn Jeong, Myeong Seon Ryu, Hee-Jong Yang, Sunmin Park
    Foods.2021; 10(2): 221.     CrossRef
  • Anti-inflammatory activities of green tea catechins along the gut–liver axis in nonalcoholic fatty liver disease: lessons learned from preclinical and human studies
    Joanna K. Hodges, Geoffrey Y. Sasaki, Richard S. Bruno
    The Journal of Nutritional Biochemistry.2020; 85: 108478.     CrossRef
  • Role of PCK1 gene on oil tea-induced glucose homeostasis and type 2 diabetes: an animal experiment and a case-control study
    Qiantu Hu, Huafeng Chen, Yanli Zuo, Qin He, Xuan He, Steve Simpson, Wei Huang, Hui Yang, Haiying Zhang, Rui Lin
    Nutrition & Metabolism.2019;[Epub]     CrossRef
  • Oil tea improves glucose and lipid levels and alters gut microbiota in type 2 diabetic mice
    Rui Lin, Xuan He, Huafeng Chen, Qin He, Ziting Yao, Yuanfan Li, Hui Yang, Steve Simpson
    Nutrition Research.2018; 57: 67.     CrossRef
  • Isomalto-oligosaccharides, a prebiotic, functionally augment green tea effects against high fat diet-induced metabolic alterations via preventing gut dysbacteriosis in mice
    Dhirendra Pratap Singh, Jagdeep Singh, Ravneet Kaur Boparai, JianHua Zhu, Shrikant Mantri, Pragyanshu Khare, Romesh Khardori, Kanthi Kiran Kondepudi, Kanwaljit Chopra, Mahendra Bishnoi
    Pharmacological Research.2017; 123: 103.     CrossRef
  • Hypoglycemic, Hypolipidemic and Antioxidant Effects of Peptides from Red Deer Antlers in Streptozotocin-Induced Diabetic Mice
    Ning Jiang, Shuangjian Zhang, Jing Zhu, Jing Shang, Xiangdong Gao
    The Tohoku Journal of Experimental Medicine.2015; 236(1): 71.     CrossRef
  • Coffee but not green tea consumption is associated with prevalence and severity of hepatic steatosis: the impact on leptin level
    T Imatoh, S Kamimura, M Miyazaki
    European Journal of Clinical Nutrition.2015; 69(9): 1023.     CrossRef
  • Green tea and type 2 diabetes
    Jae-Hyung Park, Jae-Hoon Bae, Sung-Soon Im, Dae-Kyu Song
    Integrative Medicine Research.2014; 3(1): 4.     CrossRef
  • The Effects of Green Tea on Obesity and Type 2 Diabetes
    Hyun Min Kim, Jaetaek Kim
    Diabetes & Metabolism Journal.2013; 37(3): 173.     CrossRef
Intracerebroventricular Injection of Metformin Induces Anorexia in Rats
Chang Koo Lee, Yoon Jung Choi, So Young Park, Jong Yeon Kim, Kyu Chang Won, Yong Woon Kim
Diabetes Metab J. 2012;36(4):293-299.   Published online August 20, 2012
DOI: https://doi.org/10.4093/dmj.2012.36.4.293
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  • 42 Download
  • 26 Crossref
AbstractAbstract PDFPubReader   
Background

Metformin, an oral biguanide insulin-sensitizing agent, is well known to decrease appetite. Although there is evidence that metformin could affect the brain directly, the exact mechanism is not yet known.

Methods

To evaluate whether metformin induces anorexia via the hypothalamus, various concentrations of metformin were injected into the lateral ventricle of rats through a chronically implanted catheter and food intake was measured for 24 hours. The hypothalamic neuropeptides associated with regulation of food intake were also analyzed following 1 hour of intracerebroventricular (ICV) injections of metformin.

Results

An ICV injection of metformin decreased food intake in a dose-dependent manner in unrestrained conscious rats. Hypothalamic phosphorylated AMP-activated protein kinase (pAMPK) increased by 3 µg with metformin treatment, but there was no further increase in pAMPK with increases in metformin dosage. The hypothalamic phosphorylated signal transducer and activator of transcription 3 (pSTAT3) increased by 3 µg with metformin treatment, but, there was no further increase in pSTAT3 level following increases of metformin dosage. Hypothalamic proopiomelanocortin was elevated with metformin treatment, while neuropeptide Y was not significantly changed.

Conclusion

Our results suggest that metformin induces anorexia via direct action in the hypothalamus and the increase in pSTAT3, at least in part, is involved in the process. However, hypothalamic pAMPK appears not to contribute to metformin-induced appetite reduction in normal rats. Further studies exploring new pathways connecting metformin and feeding regulation are needed.

Citations

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  • Metabolic and Metabolomic Effects of Metformin in Murine Model of Pulmonary Adenoma Formation
    Andrew C. Elton, Vannesa Cedarstrom, Arman Quraishi, Beverly Wuertz, Kevin Murray, Todd W. Markowski, Donna Seabloom, Frank G. Ondrey
    Nutrition and Cancer.2023; 75(3): 1014.     CrossRef
  • Steroidogenic Effect of Luteinizing Hormone Receptor Agonists and Metformin in Male Rats with Androgenic Deficiency Caused by Diet-Induced Obesity
    A. A. Bakhtyukov, K. V. Derkach, I. A. Lebedev, V. N. Sorokoumov, A. O. Shpakov
    Journal of Evolutionary Biochemistry and Physiology.2023; 59(5): 1810.     CrossRef
  • Metformin in nucleus accumbens core reduces cue‐induced cocaine seeking in male and female rats
    Amy Chan, Alexis Willard, Sarah Mulloy, Noor Ibrahim, Allegra Sciaccotta, Mark Schonfeld, Sade M. Spencer
    Addiction Biology.2022;[Epub]     CrossRef
  • Knockdown of Endogenous Nucb2/Nesfatin-1 in the PVN Leads to Obese-Like Phenotype and Abolishes the Metformin- and Stress-Induced Thermogenic Response in Rats
    Daniel Stephan, Natalie Taege, Riccardo Dore, Julica Folberth, Olaf Jöhren, Markus Schwaninger, Hendrik Lehnert, Carla Schulz
    Hormone and Metabolic Research.2022; 54(11): 768.     CrossRef
  • Modulation of hypothalamic AMPK phosphorylation by olanzapine controls energy balance and body weight
    Vitor Ferreira, Cintia Folgueira, Maria Guillén, Pablo Zubiaur, Marcos Navares, Assel Sarsenbayeva, Pilar López-Larrubia, Jan W. Eriksson, Maria J. Pereira, Francisco Abad-Santos, Guadalupe Sabio, Patricia Rada, Ángela M. Valverde
    Metabolism.2022; 137: 155335.     CrossRef
  • Metformin acts on the gut-brain axis to ameliorate antipsychotic-induced metabolic dysfunction
    Xiaorong Wang, Huimin Huang, Yiyi Zhu, Shaoli Li, Peifen Zhang, Jiajun Jiang, Caixi Xi, Lingling Wu, Xingle Gao, Yaoyang Fu, Danhua Zhang, Yiqing Chen, Shaohua Hu, Jianbo Lai
    BioScience Trends.2021; 15(5): 321.     CrossRef
  • Therapeutic effect of treatment with metformin and/or 4-hydroxychalcone in male Wistar rats with nonalcoholic fatty liver disease
    Selene de Jesús Acosta-Cota, Elsa Maribel Aguilar-Medina, Rosalío Ramos-Payán, José Guadalupe Rendón Maldonado, José Geovanni Romero-Quintana, Julio Montes-Avila, Juan I. Sarmiento-Sánchez, Carolina Gabriela Plazas-Guerrero, Marcela J. Vergara-Jiménez, Ar
    European Journal of Pharmacology.2019; 863: 172699.     CrossRef
  • The evidence of metabolic-improving effect of metformin in Ay/a mice with genetically-induced melanocortin obesity and the contribution of hypothalamic mechanisms to this effect
    Kira Derkach, Irina Zakharova, Inna Zorina, Andrey Bakhtyukov, Irina Romanova, Liubov Bayunova, Alexander Shpakov, Guillermo López Lluch
    PLOS ONE.2019; 14(3): e0213779.     CrossRef
  • Effect of Metformin on Antipsychotic-Induced Metabolic Dysfunction: The Potential Role of Gut-Brain Axis
    Chao Luo, Xu Wang, Hanxue Huang, Xiaoyuan Mao, Honghao Zhou, Zhaoqian Liu
    Frontiers in Pharmacology.2019;[Epub]     CrossRef
  • Metformin alters signaling induced crosstalk and homeostasis in the carcinogenesis paradigm “Epistemology of the origin of cancer”
    Björn L.D.M. Brücher, Ijaz S. Jamall, Obul R. Bandapalli
    4open.2019; 2: 12.     CrossRef
  • Melatonin potentiates the effects of metformin on glucose metabolism and food intake in high‐fat‐fed rats
    Rosana F. Dantas‐Ferreira, Helene Raingard, Stephanie Dumont, Carole Schuster‐Klein, Beatrice Guardiola‐Lemaitre, Paul Pevet, Etienne Challet
    Endocrinology, Diabetes & Metabolism.2018;[Epub]     CrossRef
  • Molecular Mechanisms of the Effects of Metformin on the Functional Activity of Brain Neurons
    A. O. Shpakov, K. V. Derkach
    Neuroscience and Behavioral Physiology.2018; 48(8): 969.     CrossRef
  • Effect of metformin/irinotecan-loaded poly-lactic-co-glycolic acid nanoparticles on glioblastoma: in vitro and in vivo studies
    Ali Taghizadehghalehjoughi, Ahmet Hacimuftuoglu, Meltem Cetin, Afife Busra Ugur, Bianca Galateanu, Yaroslav Mezhuev, Ufuk Okkay, Numan Taspinar, Mehmet Taspinar, Abdullah Uyanik, Betul Gundogdu, Maryam Mohammadzadeh, Kemal Alp Nalci, Polychronis Stivaktak
    Nanomedicine.2018; 13(13): 1595.     CrossRef
  • Effect of Betahistine and Metformin on Antipsychotic-Induced Weight Gain: An Analysis of Two Clinical Trials
    Dongyu Kang, Zhihui Jing, Ranran Li, Gangrui Hei, Tiannan Shao, Li Li, Mengxi Sun, Ye Yang, Ying Wang, Xiaoyi Wang, Yujun Long, Xiansheng Huang, Renrong Wu
    Frontiers in Psychiatry.2018;[Epub]     CrossRef
  • Metformin: not only per os
    Lev M. Berstein
    Expert Review of Endocrinology & Metabolism.2018; 13(2): 63.     CrossRef
  • МЕТАБОЛИЧЕСКИЕ ПОКАЗАТЕЛИ И ФУНКЦИОНАЛЬНОЕ СОСТОЯНИЕ СИГНАЛЬНЫХ СИСТЕМ ГИПОТАЛАМУСА И ВЛИЯНИЕ НА НИХ МЕТФОРМИНА У МЫШЕЙ С МУТАЦИЕЙ AY/A, ГЕНЕТИЧЕСКИ ПРЕДРАСПОЛОЖЕННЫХ К ОЖИРЕНИЮ, "Доклады Академии наук"
    К.В. Деркач, И.О. Захарова, И.В. Романова, И. И. Зорина, А.Л. Михрина, А.О. Шпаков
    Доклады Академии Наук.2017; (4): 488.     CrossRef
  • Beneficial effects of metformin on energy metabolism and visceral fat volume through a possible mechanism of fatty acid oxidation in human subjects and rats
    Ichiro Tokubuchi, Yuji Tajiri, Shimpei Iwata, Kento Hara, Nobuhiko Wada, Toshihiko Hashinaga, Hitomi Nakayama, Hiroharu Mifune, Kentaro Yamada, M. Faadiel Essop
    PLOS ONE.2017; 12(2): e0171293.     CrossRef
  • Metabolic parameters and functional state of hypothalamic signaling systems in AY/a mice with genetic predisposition to obesity and the effect of metformin
    K. V. Derkach, I. O. Zakharova, I. V. Romanova, I. I. Zorina, A. L. Mikhrina, A. O. Shpakov
    Doklady Biochemistry and Biophysics.2017; 477(1): 377.     CrossRef
  • Prolonged metformin treatment leads to reduced transcription of Nrf2 and neurotrophic factors without cognitive impairment in older C57BL/6J mice
    Joanne S. Allard, Evelyn J. Perez, Koji Fukui, Priscilla Carpenter, Donald K. Ingram, Rafael de Cabo
    Behavioural Brain Research.2016; 301: 1.     CrossRef
  • Intracerebroventricular Metformin Decreases Body Weight But Has Pro-oxidant Effects and Decreases Survival
    Luis Valmor Portela, Jussania Gnoatto, Andressa Wigner Brochier, Clarissa Branco Haas, Adriano Martimbianco de Assis, Afonso Kopczynski de Carvalho, Gisele Hansel, Eduardo Rigon Zimmer, Jean Pierre Oses, Alexandre Pastoris Muller
    Neurochemical Research.2015; 40(3): 514.     CrossRef
  • Metformin alleviates hepatosteatosis by restoring SIRT1-mediated autophagy induction via an AMP-activated protein kinase-independent pathway
    Young Mi Song, Yong-ho Lee, Ji-Won Kim, Dong-Sik Ham, Eun-Seok Kang, Bong Soo Cha, Hyun Chul Lee, Byung-Wan Lee
    Autophagy.2015; 11(1): 46.     CrossRef
  • Activation of AMP-activated protein kinase by metformin protects against global cerebral ischemia in male rats: Interference of AMPK/PGC-1α pathway
    Ghorbangol Ashabi, Fariba Khodagholi, Leila Khalaj, Mahdi Goudarzvand, Masoumeh Nasiri
    Metabolic Brain Disease.2014; 29(1): 47.     CrossRef
  • Acute oral metformin enhances satiation and activates brainstem nesfatinergic neurons
    Thaïs Rouquet, Pierre Clément, Stéphanie Gaigé, Catherine Tardivel, Julien Roux, Michel Dallaporta, Bruno Bariohay, Jean-Denis Troadec, Bruno Lebrun
    Obesity.2014; : n/a.     CrossRef
  • Metformin—mode of action and clinical implications for diabetes and cancer
    Ida Pernicova, Márta Korbonits
    Nature Reviews Endocrinology.2014; 10(3): 143.     CrossRef
  • Effects of metformin on weight loss
    Steven K. Malin, Sangeeta R. Kashyap
    Current Opinion in Endocrinology, Diabetes & Obesity.2014; 21(5): 323.     CrossRef
  • The effect of ghrelin on MK-801 induced memory impairment in rats
    Fatemeh Goshadrou, Mojtaba Kermani, Abdolaziz Ronaghi, Samad Sajjadi
    Peptides.2013; 44: 60.     CrossRef
ATP-Sensitive Potassium Channel-Deficient Mice Show Hyperphagia but Are Resistant to Obesity
Yeul Bum Park, Yun Jung Choi, So Young Park, Jong Yeon Kim, Seong Ho Kim, Dae Kyu Song, Kyu Chang Won, Yong Woon Kim
Diabetes Metab J. 2011;35(3):219-225.   Published online June 30, 2011
DOI: https://doi.org/10.4093/dmj.2011.35.3.219
  • 3,499 View
  • 31 Download
  • 14 Crossref
AbstractAbstract PDFPubReader   
Background

The hypothalamus, the center for body weight regulation, can sense changes in blood glucose level based on ATP-sensitive potassium (KATP) channels in the hypothalamic neurons. We hypothesized that a lack of glucose sensing in the hypothalamus affects the regulations of appetite and body weight.

Methods

To evaluate this hypothesis, the responses to glucose loading and high fat feeding for eight weeks were compared in Kir6.2 knock-out (KO) mice and control C57BL/6 mice, because Kir6.2 is a key component of the KATP channel.

Results

The hypothalamic neuropeptide Y (NPY) analyzed one hour after glucose injection was suppressed in C57BL/6 mice, but not in Kir6.2 KO mice, suggesting a blunted hypothalamic response to glucose in Kir6.2 KO mice. The hypothalamic NPY expression at a fed state was elevated in Kir6.2 KO mice and was accompanied with hyperphagia. However, the retroperitoneal fat mass was markedly decreased in Kir6.2 KO mice compared to that in C57BL/6 mice. Moreover, the body weight and visceral fat following eight weeks of high fat feeding in Kir6.2 KO mice were not significantly different from those in control diet-fed Kir6.2 KO mice, while body weight and visceral fat mass were elevated due to high fat feeding in C57BL/6 mice.

Conclusion

These results suggested that Kir6.2 KO mice showed a blunted hypothalamic response to glucose loading and elevated hypothalamic NPY expression accompanied with hyperphagia, while visceral fat mass was decreased, suggesting resistance to diet-induced obesity. Further study is needed to explain this phenomenon.

Citations

Citations to this article as recorded by  
  • 17β-estradiol promotes acute refeeding in hungry mice via membrane-initiated ERα signaling
    Kaifan Yu, Yanlin He, Ilirjana Hyseni, Zhou Pei, Yongjie Yang, Pingwen Xu, Xing Cai, Hesong Liu, Na Qu, Hailan Liu, Yang He, Meng Yu, Chen Liang, Tingting Yang, Julia Wang, Pierre Gourdy, Jean-Francois Arnal, Francoise Lenfant, Yong Xu, Chunmei Wang
    Molecular Metabolism.2020; 42: 101053.     CrossRef
  • Brain Glucose-Sensing Mechanism and Energy Homeostasis
    A. J. López-Gambero, F. Martínez, K. Salazar, M. Cifuentes, F. Nualart
    Molecular Neurobiology.2019; 56(2): 769.     CrossRef
  • The involvement of purinergic signalling in obesity
    Geoffrey Burnstock, Daniela Gentile
    Purinergic Signalling.2018; 14(2): 97.     CrossRef
  • High‐fat‐diet‐induced remission of diabetes in a subset of KATP‐GOF insulin‐secretory‐deficient mice
    Zihan Yan, Zeenat A. Shyr, Manuela Fortunato, Alecia Welscher, Mariana Alisio, Michael Martino, Brian N. Finck, Hannah Conway, Maria S. Remedi
    Diabetes, Obesity and Metabolism.2018; 20(11): 2574.     CrossRef
  • Hypothalamic arcuate nucleus glucokinase regulates insulin secretion and glucose homeostasis
    Yue Ma, Risheka Ratnasabapathy, Chioma Izzi‐Engbeaya, Marie‐Sophie Nguyen‐Tu, Errol Richardson, Sufyan Hussain, Ivan De Backer, Christopher Holton, Mariana Norton, Gaelle Carrat, Blanche Schwappach, Guy A. Rutter, Waljit S. Dhillo, James Gardiner
    Diabetes, Obesity and Metabolism.2018; 20(9): 2246.     CrossRef
  • Overexpression of WNK1 in POMC-expressing neurons reduces weigh gain via WNK4-mediated degradation of Kir6.2
    Woo Young Chung, Jung Woo Han, Woon Heo, Min Goo Lee, Joo Young Kim
    Molecular and Cellular Biochemistry.2018; 447(1-2): 165.     CrossRef
  • Insights into the role of neuronal glucokinase
    Ivan De Backer, Sufyan S. Hussain, Stephen R. Bloom, James V. Gardiner
    American Journal of Physiology-Endocrinology and Metabolism.2016; 311(1): E42.     CrossRef
  • Obesogenic and Diabetogenic Effects of High-Calorie Nutrition Require Adipocyte BK Channels
    Julia Illison, Lijun Tian, Heather McClafferty, Martin Werno, Luke H. Chamberlain, Veronika Leiss, Antonia Sassmann, Stefan Offermanns, Peter Ruth, Michael J. Shipston, Robert Lukowski
    Diabetes.2016; 65(12): 3621.     CrossRef
  • ABCC8 R1420H Loss-of-Function Variant in a Southwest American Indian Community: Association With Increased Birth Weight and Doubled Risk of Type 2 Diabetes
    Leslie J. Baier, Yunhua Li Muller, Maria Sara Remedi, Michael Traurig, Paolo Piaggi, Gregory Wiessner, Ke Huang, Alyssa Stacy, Sayuko Kobes, Jonathan Krakoff, Peter H. Bennett, Robert G. Nelson, William C. Knowler, Robert L. Hanson, Colin G. Nichols, Clif
    Diabetes.2015; 64(12): 4322.     CrossRef
  • Glucokinase activity in the arcuate nucleus regulates glucose intake
    Syed Hussain, Errol Richardson, Yue Ma, Christopher Holton, Ivan De Backer, Niki Buckley, Waljit Dhillo, Gavin Bewick, Shuai Zhang, David Carling, Steve Bloom, James Gardiner
    Journal of Clinical Investigation.2015; 125(1): 337.     CrossRef
  • Dissecting the Etiology of Type 2 Diabetes in the Pima Indian Population
    Ewan R. Pearson
    Diabetes.2015; 64(12): 3993.     CrossRef
  • Ocular Hypotensive Effects of the ATP-Sensitive Potassium Channel Opener Cromakalim in Human and Murine Experimental Model Systems
    Uttio Roy Chowdhury, Cindy K. Bahler, Bradley H. Holman, Peter I. Dosa, Michael P. Fautsch, Ted S Acott
    PLOS ONE.2015; 10(11): e0141783.     CrossRef
  • Differential gene expression pattern in hypothalamus of chickens during fasting-induced metabolic reprogramming: Functions of glucose and lipid metabolism in the feed intake of chickens
    Xin-Ling Fang, Xiao-Tong Zhu, Sheng-Feng Chen, Zhi-Qi Zhang, Qing-Jie Zeng, Lin Deng, Jian-Long Peng, Jian-Jian Yu, Li-Na Wang, Song-Bo Wang, Ping Gao, Qing-Yan Jiang, Gang Shu
    Poultry Science.2014; 93(11): 2841.     CrossRef
  • Combined Treatment of Betulinic Acid, a PTP1B Inhibitor, with Orthosiphon stamineus Extract Decreases Body Weight in High-Fat–Fed Mice
    Yoon-Jung Choi, So-Young Park, Jong-Yeon Kim, Kyu-Chang Won, Bo-Ra Kim, Jong-Keun Son, Seung-Ho Lee, Yong-Woon Kim
    Journal of Medicinal Food.2013; 16(1): 2.     CrossRef
Differential Effects of Palmitate and Docosahexaenoic acid on ATP-sensitive K+ Channel Activity of Pancreatic beta-cells.
Yong Woon Kim, Kyeung Oh Doh, Dae Kyu Song, Jae Hoon Bae, Won Kyun Park, Kyu Jang Won, Hyoung Woo Lee, Suck Kang Lee
Korean Diabetes J. 1999;23(6):768-776.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Elevated levels of free fatty acids markedly enhance insulin secretion. However, dietary polyunsaturated fatty supplementation decrease insulin secretion. The effects of different type of fatty acids on cultured pancreatic beta cell remain controversy. Therefore, the specific goal of this study was to confirm the effect of palmitate and docosahexaenoic acid (DHA) on pancreatic beta-cells. We measured ATP-sensitive K+ (KATP) channel activity by patch clamp technique. METHOD: Pancreatic beta-cells were isolated from male Sprague-Dawley rats and cultured on the cover glass in the culture media. KATP channel activity of pancreatic beta-cells were measured by the cell-attached mode of the patch clamp technique. We treated 30 micrometer of palmitate and DHA dissolved with 3% albumin solution. RESULT: 30 micrometer of palmitate inhibited KATP channel activity. Moreover, after additions of 5 and 10 mM glucose, additional and dose dependent inhibitory effects were revealed. However, 30 micrometer of DHA did not have these additional inhibitory effect treated with 5 and lOmM glucose. CONCLUSION: Palmitate as a saturated fatty acid inhibited activity of KATP channel and increased inhibitory effect of glucose on this channel activity, however, DHA as a polyunsaturated fatty acid attenuated inhibitory effect of glucose on this channel activity.
Effect of w-3 polyunsaturated fatty acids supplementation diet oninsulin binding, and generation of diabetes in STZ-injected femalerats.
Suck Kang Lee, Jong Yeon Kim, Yong Woon Kim, Gong Rae Cho
Korean Diabetes J. 1992;16(2):103-110.   Published online January 1, 2001
  • 800 View
  • 17 Download
AbstractAbstract PDF
No abstract available.
Insulin resistance on receptor and post-receptor phases in streptozotocin-induced diabetes rats.
Jong Yeon Kim, Yong Woon Kim, Suck Kang Lee
Korean Diabetes J. 1991;15(1):53-62.   Published online January 1, 2001
  • 763 View
  • 16 Download
AbstractAbstract PDF
No abstract available.

Diabetes Metab J : Diabetes & Metabolism Journal