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High Fat Diet Induced Insulin Resistance

Increased Oxidative Stress Precedes The Onset Of High-fat Dietinduced Insulin Resistance And Obesity

Increased Oxidative Stress Precedes The Onset Of High-fat Dietinduced Insulin Resistance And Obesity

Volume 57, Issue 8 , August 2008, Pages 1071-1077 Increased oxidative stress precedes the onset of high-fat dietinduced insulin resistance and obesity Author links open overlay panel NaotoMatsuzawa-Nagataab ToshinariTakamurab Get rights and content Insulin resistance is a key pathophysiological feature of metabolic syndrome. However, the initial events triggering the development of insulin resistance and its causal relations with dysregulation of glucose and fatty acids metabolism remain unclear. We investigated biological pathways that have the potential to induce insulin resistance in mice fed a high-fat diet (HFD). We demonstrate that the pathways for reactive oxygen species (ROS) production and oxidative stress are coordinately up-regulated in both the liver and adipose tissue of mice fed an HFD before the onset of insulin resistance through discrete mechanism. In the liver, an HFD up-regulated genes involved in sterol regulatory element binding protein 1crelated fatty acid synthesis and peroxisome proliferatoractivated receptor related fatty acid oxidation. In the adipose tissue, however, the HFD down-regulated genes involved in fatty acid synthesis and up-regulated nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex. Furthermore, increased ROS production preceded the elevation of tumor necrosis factor and free fatty acids in the plasma and liver. The ROS may be an initial key event triggering HFD-induced insulin resistance. Continue reading >>

Myeloid Cell Neuropilin 1 Ameliorates High-fat Diet-induced Insulin Resistance Via Suppression Of Nlrp3 Inflammasome | Dai | Macrophage

Myeloid Cell Neuropilin 1 Ameliorates High-fat Diet-induced Insulin Resistance Via Suppression Of Nlrp3 Inflammasome | Dai | Macrophage

Myeloid cell neuropilin 1 ameliorates high-fat diet-induced insulin resistance via suppression of Nlrp3 inflammasome The history of neuropilin 1 (Nrp1) research is checkered with many unexpected and exciting findings. Originally identified as a co-receptor for class 3 semaphorins, and several canonical growth factors, Nrp1 was shown to play important roles in the development of central nervous system, and angiogenesis within neuronal and endothelial cells, respectively. Accumulating evidence demonstrates that Nrp1 is also highly expressed in immune cells, including macrophages and dendritic cells. Until now, the functions of Nrp1 within these cells remained poorly studied and elusive. In this research highlight, we provide exciting insights on our recently published study that identified a novel role for myeloid cell Nrp1 in the mitigation of high-fat diet-induced insulin resistance via suppression of Nlrp3 inflammasome. Johnson AM, Olefsky JM. The origins and drivers of insulin resistance. Cell 2013; 152:673-684. Qatanani M, Lazar MA. Mechanisms of obesity-associated insulin resistance: many choices on the menu. Genes & development 2007; 21:1443-1455. Stepanova OI, Krylov AV, Lioudyno VI, Kisseleva EP. Gene expression for VEGF-A, VEGF-C, and their receptors in murine lymphocytes and macrophages. Biochemistry (Mosc) 2007; 72:1194-1198. Casazza A, Laoui D, Wenes M, Rizzolio S, Bassani N, Mambretti M, et al. Impeding macrophage entry into hypoxic tumor areas by Sema3A/Nrp1 signaling blockade inhibits angiogenesis and restores antitumor immunity. Cancer cell 2013; 24:695-709. Miyauchi JT, Chen D, Choi M, Nissen JC, Shroyer KR, Djordevic S, et al. Ablation of Neuropilin 1 from glioma-associated microglia and macrophages slows tumor progression. Oncotarget 2016; 7:9801-9814 Continue reading >>

Imidacloprid Promotes High Fat Diet-induced Adiposity And Insulin Resistance In Male C57bl/6j Mice

Imidacloprid Promotes High Fat Diet-induced Adiposity And Insulin Resistance In Male C57bl/6j Mice

Imidacloprid Promotes High Fat Diet-Induced Adiposity and Insulin Resistance in Male C57BL/6J Mice Department of Food Science, University of Massachusetts, Amherst, Massachusetts 01003, United States Department of Mathematics and Statistics, University of Massachusetts, Amherst, Massachusetts 01003, United States Department of Biological Sciences and Environmental Sciences Program, Southern Illinois University, Edwardsville, Illinois 62026, United States # Department of Veterinary and Animal Sciences, University of Massachusetts, Amherst, Massachusetts 01003, United States *(Y.P.) Mail: Department of Food Science, University of Massachusetts, 102 Holdsworth Way, Amherst, MA 01003, USA. Phone: (413) 545-1018. Fax: (413) 545-1262. E-mail: [emailprotected] . Cite this: J. Agric. Food Chem. 2016, 64, 49, 9293-9306 Article Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days. Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts. The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Imidacloprid, a neonicotinoid insecticide widely used in agriculture worldwide, has been reported to promote adipogenesis and cause insulin resistance in vitro. The purpose of the current study was to determine the Continue reading >>

Ethanol Extract From Ulva Prolifera Prevents High-fat Diet-induced Insulin Resistance, Oxidative Stress, And Inflammation Response In Mice

Ethanol Extract From Ulva Prolifera Prevents High-fat Diet-induced Insulin Resistance, Oxidative Stress, And Inflammation Response In Mice

Ethanol Extract from Ulva prolifera Prevents High-Fat Diet-Induced Insulin Resistance, Oxidative Stress, and Inflammation Response in Mice Wei Song ,1,2 Zongling Wang ,1,2 Xuelei Zhang ,1,2 and Yan Li 1,2 1Key Laboratory of Science and Engineering for Marine Ecology and Environment, The First Institute of Oceanography, SOA, Qingdao 266061, China 2Laboratory of Marine Ecology and Environmental Science, Qingdao National Laboratory for Marine Science and Technology, Qingdao 266235, China Correspondence should be addressed to Zongling Wang ; nc.gro.oif@lzgnaw Received 13 November 2017; Accepted 17 December 2017; Published 3 January 2018 Copyright 2018 Wei Song et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Ulva prolifera is the major causative species in the green tide, a serious marine ecological disaster, which bloomed in the Yellow Sea and the Bohai Sea of China. However, it is also a popular edible seaweed and its extracts exerts anti-inflammatory and antioxidant effects. The present study investigated the effects of ethanol extract of U. prolifera (EUP) on insulin sensitivity, inflammatory response, and oxidative stress in high-fat-diet- (HFD-) treated mice. HFD-treated mice obtained drinking water containing 2% or 5% EUP. The results showed that EUP supplementation significantly prevented HFD-induced weight gain of liver and fat. EUP supplementation also improved glucose tolerance and insulin resistance in HFD-treated mice. Moreover, EUP supplementation prevented the increased expression of genes involved in triglyceride synthesis and proinflammatory genes and the decreased expression of genes Continue reading >>

High-fructose And High-fat Diet-induced Insulin Resistance Enhances Atherosclerosis In Watanabe Heritable Hyperlipidemic Rabbits

High-fructose And High-fat Diet-induced Insulin Resistance Enhances Atherosclerosis In Watanabe Heritable Hyperlipidemic Rabbits

High-fructose and high-fat diet-induced insulin resistance enhances atherosclerosis in Watanabe heritable hyperlipidemic rabbits Individuals with insulin resistance and resulting impaired glucose tolerance along with type 2 diabetes showed an increased prevalence of atherosclerosis. Our aim in this study was to address whether diet-induced insulin resistance plays any roles in the development of aortic and coronary atherosclerosis in hyperlipidemic rabbits. We fed Watanabe heritable hyperlipidemic (WHHL) rabbits with a high-fructose and high-fat diet (HFFD) with restricted normal calories and compared the lesions of both aortic and coronary atherosclerosis with those of control WHHL rabbits fed a normal chow diet. HFFD-fed WHHL rabbits showed insulin resistance and impaired glucose tolerance accompanied by elevated plasma lipid levels and accumulation of adipose tissue even though their body weight was unchanged compared to the control rabbits. At 8 weeks, the aortic gross lesion area of HFFD-fed WHHL rabbits was increased by 40 % over the controls and their lesions were characterized by increased number of macrophages and smooth muscle cells. At 16 weeks, the lesions of HFFD-fed WHHL rabbits showed more advanced lesions such as lipid core formation and calcification. In addition, coronary atherosclerosis was significantly increased in HFFD-fed WHHL rabbits. These results suggest that insulin resistance accelerates lesion formation of atherosclerosis. Insulin ResistanceCoronary AtherosclerosisCholesteryl Ester Transfer ProteinMicrosomal Triglyceride Transfer ProteinAdvanced Lesion Insulin resistance (IR) is frequently associated with many metabolic diseases such as obesity, hypertriglyceridemia, type 2 diabetes, and metabolic syndrome [ 1 ]. Individuals with underlying Continue reading >>

Association Of Muscle Lipidomic Profile With High-fat Diet-induced Insulin Resistance Across Five Mouse Strains.

Association Of Muscle Lipidomic Profile With High-fat Diet-induced Insulin Resistance Across Five Mouse Strains.

Association of muscle lipidomic profile with high-fat diet-induced insulin resistance across five mouse strains. Recommended by Amira Klip and Nicolas Pillon 09 Nov 2017 | Confirmation, Controversial Montgomery and colleagues used lipidomics to describe changes in skeletal muscle lipid profiles in five different strains of mice (C57BL6, 129X1, DBA/2, FVB/N, and BALB/c) subjected to a high-fat diet for 8 weeks. In a previous study, the authors had shown that all except BALB/c mice gain weight and develop glucose intolerance in that time {1}. Here, a comprehensive analysis revealed that in muscle, triglycerides... To read the rest of this recommendation and access over 145,000 article recommendations from 3,700+ journals across biomedicine, register Send a recommendation to your institution's librarian or information manager to request an extended free trial for articles in biology and medicine, contributed inclusion in F1000Prime to help you filter recommendations, plus relevant articles as engine clusters of related articles and be alerted as soon as similar articles appear in If you think you should be able to access this content, please contact us . If you've forgotten your password, please enter your email address below and we'll send you instructions on how to reset your password. The email address should be the one you originally registered with F1000. Email address not recognised, please try again We are unable to reset your password, please contact [email protected] to reactivate your account, quoting error code UACC/DEL You registered with F1000 via Google, so we cannot reset your password. If you still need help with your Google account password, please click here . You registered with F1000 via Facebook, so we cannot reset your password. If you still need help w Continue reading >>

Effects Of The Green Tea Polyphenol Epigallocatechin-3-gallate On High-fat Diet-induced Insulin Resistance And Endothelial Dysfunction

Effects Of The Green Tea Polyphenol Epigallocatechin-3-gallate On High-fat Diet-induced Insulin Resistance And Endothelial Dysfunction

Effects of the green tea polyphenol epigallocatechin-3-gallate on high-fat diet-induced insulin resistance and endothelial dysfunction Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of Alabama at Birmingham, Birmingham, Alabama; Department of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, Birmingham, Alabama; and Comprehensive Diabetes Center, University of Alabama at Birmingham, Birmingham, Alabama *Both of these authors contributed equally to this work.Address for reprint requests and other correspondence: J. A. Kim, Dept. of Medicine, Div. of Endocrinology, Diabetes, and Metabolism, Univ. of Alabama at Birmingham, Birmingham, AL 35294 (e-mail: E-mail Address: [emailprotected] ). Insulin resistance, a hallmark of metabolic disorders, is a risk factor for diabetes and cardiovascular disease. Impairment of insulin responsiveness in vascular endothelium contributes to insulin resistance. The reciprocal relationship between insulin resistance and endothelial dysfunction augments the pathophysiology of metabolism and cardiovascular functions. The most abundant green tea polyphenol, epigallocatechin-3-gallate (EGCG), has been shown to have vasodilator action in vessels by activation of endothelial nitric oxide synthase (eNOS). However, it is not known whether EGCG has a beneficial effect in high-fat diet (HFD)-induced endothelial dysfunction. Male C57BL/6J mice were fed either a normal chow diet (NCD) or HFD with or without EGCG supplement (50 mgkg1day1) for 10 wk. Mice fed a HFD with EGCG supplement gained less body weight and showed improved insulin sensitivity. In vehicle-treated HFD mice, endothelial function was impaired in response to insulin but not to acetylcholine, whereas the EGCG-treate Continue reading >>

Tetradecylthioacetic Acid Prevents High Fat Diet Induced Adiposity And Insulin Resistance

Tetradecylthioacetic Acid Prevents High Fat Diet Induced Adiposity And Insulin Resistance

Tetradecylthioacetic acid prevents high fat diet induced adiposity and insulin resistance *Department of Clinical Biochemistry, University of Bergen, Haukeland Hospital, N-5021 Bergen, Norway U465 INSERM, Institut Biomdical des Cordeliers, Paris, France Department of Biochemistry and Molecular Biology, University of Southern Denmark, DK-5230 Odense M, Denmark **Diabetes and Nutrition Research Laboratory, Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Slovak Republic Department of Pharmacology, School of Pharmacy, University of Oslo, Oslo, Norway National Institute of Occupational Health, Oslo, Norway ***UR545 INSERM, Department d'Athrosclerose, Institut Pasteur de Lille and Facult de Pharmacie, Universit de Lille II, Lille, France 1To whom correspondence should be addressed. e-mail: rolf.berge{at}ikb.uib.no Tetradecylthioacetic acid (TTA) is a non--oxidizable fatty acid analog, which potently regulates lipid homeostasis. Here we evaluate the ability of TTA to prevent diet-induced and genetically determined adiposity and insulin resistance. In Wistar rats fed a high fat diet, TTA administration completely prevented diet-induced insulin resistance and adiposity. In genetically obese Zucker (fa/fa) rats TTA treatment reduced the epididymal adipose tissue mass and improved insulin sensitivity. All three rodent peroxisome proliferator-activated receptor (PPAR) subtypes were activated by TTA in the ranking order PPAR > PPAR > PPAR. Expression of PPAR target genes in adipose tissue was unaffected by TTA treatment, whereas the hepatic expression of PPAR-responsive genes encoding enzymes involved in fatty acid uptake, transport, and oxidation was induced. This was accompanied by increased hepatic mitochondrial -oxidation and a decreased fatty a Continue reading >>

High-fat Diet Induces Hepatic Insulin Resistance And Impairment Of Synaptic Plasticity

High-fat Diet Induces Hepatic Insulin Resistance And Impairment Of Synaptic Plasticity

High-Fat Diet Induces Hepatic Insulin Resistance and Impairment of Synaptic Plasticity Zhigang Liu , Ishan Y. Patil , Tianyi Jiang , Harsh Sancheti , John P. Walsh , Bangyan L. Stiles , Fei Yin , Enrique Cadenas Affiliations: Pharmacology & Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA, 90089, United States of America, College of Food Science and Engineering, Northwest A&F University, Yangling, China Affiliation: Pharmacology & Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA, 90089, United States of America Affiliation: Pharmacology & Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA, 90089, United States of America Affiliation: Pharmacology & Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA, 90089, United States of America Affiliation: Davis School of Gerontology and Program in Neuroscience, University of Southern California, Los Angeles, CA, 90089, United States of America Affiliation: Pharmacology & Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA, 90089, United States of America Affiliation: Pharmacology & Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA, 90089, United States of America Affiliation: Pharmacology & Pharmaceutical Sciences, School of Pharmacy, University of Southern California, Los Angeles, CA, 90089, United States of America High-fat diet (HFD)-induced obesity is associated with insulin resistance, which may affect brain synaptic plasticity through impairment of insulin-sensitive processes underlying neuronal survival, learning, and memory. The experimental model consis Continue reading >>

High-fat Diet-induced Insulin Resistance In Single Skeletal Muscle Fibers Is Fiber Type Selective

High-fat Diet-induced Insulin Resistance In Single Skeletal Muscle Fibers Is Fiber Type Selective

N2 - Skeletal muscle is the major site for insulin-stimulated glucose disposal, and muscle insulin resistance confers many negative health outcomes. Muscle is composed of multiple fiber types, and conventional analysis of whole muscles cannot elucidate fiber type differences at the cellular level. Previous research demonstrated that a brief (two weeks) high fat diet (HFD) caused insulin resistance in rat skeletal muscle. The primary aim of this study was to determine in rat skeletal muscle the influence of a brief (two weeks) HFD on glucose uptake (GU) insulin in single fibers that were also characterized for fiber type. Epitrochlearis muscles were incubated with [3H]-2-deoxyglucose (2DG) 100 U/ml insulin. Fiber type (myosin heavy chain expression) and 2DG accumulation were measured in whole muscles and single fibers. Although fiber type composition of whole muscles did not differ between diet groups, GU of insulin-stimulated whole muscles from LFD rats significantly exceeded HFD values (P < 0.005). For HFD versus LFD rats, GU of insulin-stimulated single fibers was significantly (P < 0.05) lower for IIA, IIAX, IIBX, IIB, and approached significance for IIX (P = 0.100), but not type I (P = 0.776) fibers. These results revealed HFD-induced insulin resistance was attributable to fiber type selective insulin resistance and independent of altered fiber type composition. AB - Skeletal muscle is the major site for insulin-stimulated glucose disposal, and muscle insulin resistance confers many negative health outcomes. Muscle is composed of multiple fiber types, and conventional analysis of whole muscles cannot elucidate fiber type differences at the cellular level. Previous research demonstrated that a brief (two weeks) high fat diet (HFD) caused insulin resistance in rat sk Continue reading >>

High-fat Diet-induced Insulin Resistance In Single Skeletal Muscle Fibers Is Fiber Type Selective

High-fat Diet-induced Insulin Resistance In Single Skeletal Muscle Fibers Is Fiber Type Selective

Skeletal muscle is the major site for insulin-stimulated glucose disposal, and muscle insulin resistance confers many negative health outcomes. Muscle is composed of multiple fiber types, and conventional analysis of whole muscles cannot elucidate fiber type differences at the cellular level. Previous research demonstrated that a brief (two weeks) high fat diet (HFD) caused insulin resistance in rat skeletal muscle. The primary aim of this study was to determine in rat skeletal muscle the influence of a brief (two weeks) HFD on glucose uptake (GU) ± insulin in single fibers that were also characterized for fiber type. Epitrochlearis muscles were incubated with [3H]-2-deoxyglucose (2DG) ± 100 µU/ml insulin. Fiber type (myosin heavy chain expression) and 2DG accumulation were measured in whole muscles and single fibers. Although fiber type composition of whole muscles did not differ between diet groups, GU of insulin-stimulated whole muscles from LFD rats significantly exceeded HFD values (P < 0.005). For HFD versus LFD rats, GU of insulin-stimulated single fibers was significantly (P < 0.05) lower for IIA, IIAX, IIBX, IIB, and approached significance for IIX (P = 0.100), but not type I (P = 0.776) fibers. These results revealed HFD-induced insulin resistance was attributable to fiber type selective insulin resistance and independent of altered fiber type composition. Skeletal muscle is the major site for insulin-stimulated glucose disposal1, and skeletal muscle insulin resistance is a primary and essential event in the progression to type 2 diabetes2. Even in the absence of type 2 diabetes, insulin resistance confers negative health outcomes3. It is important to understand the processes responsible for insulin resistance of the skeletal muscle to develop interventions Continue reading >>

The Intestinal/liver Axis In The Capacity Of Anthocyanidins To Mitigate High Fat Diet-induced Insulin Resistance - Sciencedirect

The Intestinal/liver Axis In The Capacity Of Anthocyanidins To Mitigate High Fat Diet-induced Insulin Resistance - Sciencedirect

Get rights and content An increased permeability of the intestinal barrier is proposed as one underlying factor of obesity-associated pathologies. Consumption of high fat diet (HFD) is associated with intestinal permeabilization and increased paracellular transport of endotoxins, which can promote steatosis and insulin resistance. We investigated the capacity of dietary anthocyanidins (AC) to mitigate steatosis and improve insulin sensitivity in HFD-fed mice. Male C57BL/6J mice were fed for 14 w control (C) or high fat (HF) diet, with or without supplementation with 2, 20, or 40mg/kg BW of a blend of AC-rich plant extracts (ACE). The consumption of HFD caused overweight and insulin resistance, which were mitigated by ACE consumption. Concurrently, ACE prevented HFD-induced intestinal permeabilization, altered expression of ileum tight junction proteins (decreased ZO-1 and occludin) and endotoxemia. AC protection of barrier permeability is in part due to the inhibition of HFD-induced ileum ERK1/2 and AMPK activation, increased GLP-2 levels, and mitigation of dysbiosis. Consistently, the highest AC dose prevented steatosis and improved blood and liver inflammation and oxidative stress. Findings suggest that ACE supplementation could be an important strategy to mitigate obesity and Western style diets-associated insulin resistance in part through the preservation of intestinal barrier integrity. Continue reading >>

Inflammation Is Necessary For Long-term But Not Short-term High-fat Diet-induced Insulin Resistance

Inflammation Is Necessary For Long-term But Not Short-term High-fat Diet-induced Insulin Resistance

Inflammation is necessary for long-term but not short-term high-fat diet-induced insulin resistance OBJECTIVE Tissue inflammation is a key factor underlying insulin resistance in established obesity. Several models of immuno-compromised mice are protected from obesity-induced insulin resistance. However, it is unanswered whether inflammation triggers systemic insulin resistance or vice versa in obesity. The purpose of this study was to assess these questions. RESEARCH DESIGN AND METHODS We fed a high-fat diet (HFD) to wild-type mice and three different immuno-compromised mouse models (lymphocyte-deficient Rag1 knockout, macrophage-depleted, and hematopoietic cell-specific Jun NH(2)-terminal kinase-deficient mice) and measured the time course of changes in macrophage content, inflammatory markers, and lipid accumulation in adipose tissue, liver, and skeletal muscle along with systemic insulin sensitivity. RESULTS In wild-type mice, body weight and adipose tissue mass, as well as insulin resistance, were clearly increased by 3 days of HFD. Concurrently, in the short-term HFD period inflammation was selectively elevated in adipose tissue. Interestingly, however, all three immuno-compromised mouse models were not protected from insulin resistance induced by the short-term HFD. On the other hand, lipid content was markedly increased in liver and skeletal muscle at day 3 of HFD. CONCLUSIONS These data suggest that the initial stage of HFD-induced insulin resistance is independent of inflammation, whereas the more chronic state of insulin resistance in established obesity is largely mediated by macrophage-induced proinflammatory actions. The early-onset insulin resistance during HFD feeding is more likely related to acute tissue lipid overload. OBJECTIVE Tissue inflammation i Continue reading >>

Estrogens Protect Against High-fat Diet-induced Insulin Resistance And Glucose Intolerance In Mice

Estrogens Protect Against High-fat Diet-induced Insulin Resistance And Glucose Intolerance In Mice

Estrogens Protect against High-Fat Diet-Induced Insulin Resistance and Glucose Intolerance in Mice Team 9 (E.R., H.C., J.-F.A., P.G.), Institut National de la Sante et de la Recherche Medicale (INSERM) Unite 858 et Universite de Toulouse, Institut de Medecine Moleculaire de Rangueil, Institut Federatif de Recherche (IFR) 31, Toulouse, France Department of Team 2 (E.R., A.W., R.B.), INSERM Unite 858, Institut de Medecine Moleculaire de Rangueil, IFR31, 31432 Toulouse, France Search for other works by this author on: Department of Team 2 (E.R., A.W., R.B.), INSERM Unite 858, Institut de Medecine Moleculaire de Rangueil, IFR31, 31432 Toulouse, France Search for other works by this author on: Team 9 (E.R., H.C., J.-F.A., P.G.), Institut National de la Sante et de la Recherche Medicale (INSERM) Unite 858 et Universite de Toulouse, Institut de Medecine Moleculaire de Rangueil, Institut Federatif de Recherche (IFR) 31, Toulouse, France Search for other works by this author on: Team 9 (E.R., H.C., J.-F.A., P.G.), Institut National de la Sante et de la Recherche Medicale (INSERM) Unite 858 et Universite de Toulouse, Institut de Medecine Moleculaire de Rangueil, Institut Federatif de Recherche (IFR) 31, Toulouse, France Search for other works by this author on: Department of Team 2 (E.R., A.W., R.B.), INSERM Unite 858, Institut de Medecine Moleculaire de Rangueil, IFR31, 31432 Toulouse, France Search for other works by this author on: Team 9 (E.R., H.C., J.-F.A., P.G.), Institut National de la Sante et de la Recherche Medicale (INSERM) Unite 858 et Universite de Toulouse, Institut de Medecine Moleculaire de Rangueil, Institut Federatif de Recherche (IFR) 31, Toulouse, France Service de Diabetologie (P.G.), Pole Cardio-Vasculaire et Metabolique, Centre Hospitalier Universitaire d Continue reading >>

Catalpol Ameliorates High-fat Diet-induced Insulin Resistance And Adipose Tissue Inflammation By Suppressing The Jnk And Nf-b Pathways

Catalpol Ameliorates High-fat Diet-induced Insulin Resistance And Adipose Tissue Inflammation By Suppressing The Jnk And Nf-b Pathways

Volume 467, Issue 4 , 27 November 2015, Pages 853-858 Catalpol ameliorates high-fat diet-induced insulin resistance and adipose tissue inflammation by suppressing the JNK and NF-B pathways Catalpol ameliorates high-fat diet (HFD)-induced insulin resistance in mice. Catalpol reduces adipose tissue macrophage infiltration in HFD-fed mice. Catalpol regulates M1 and M2 inflammatory gene expression in obese adipose tissue. Catalpol suppresses the JNK and NF-B signaling pathways in obese adipose tissue. Catalpol, a bioactive component from the root of Rehmannia glutinosa, has been shown to possess hypoglycemic effects in type 2 diabetic animal models, however, the underlying mechanisms remain poorly understood. Here we investigated the effect of catalpol on high-fat diet (HFD)-induced insulin resistance and adipose tissue inflammation in mice. Oral administration of catalpol at 100mg/kg for 4 weeks had no effect on body weight of HFD-induced obese mice, but it significantly improved fasting glucose and insulin levels, glucose tolerance and insulin tolerance. Moreover, macrophage infiltration into adipose tissue was markedly reduced by catalpol. Intriguingly, catalpol also significantly reduced mRNA expressions of M1 pro-inflammatory cytokines, but increased M2 anti-inflammatory gene expressions in adipose tissue. Concurrently, catalpol significantly suppressed the c-Jun NH2-terminal kinase (JNK) and nuclear factor-kappa B (NF-B) signaling pathways in adipose tissue. Collectively, these results suggest that catalpol may ameliorate HFD-induced insulin resistance in mice by attenuating adipose tissue inflammation and suppressing the JNK and NF-B pathways, and thus provide important new insights into the underlying mechanisms of the antidiabetic effect of catalpol. Continue reading >>

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