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High Fat Diet Induced Insulin Resistance

Senna Alata Leaf Extract Restores Insulin Sensitivity In High-fat Diet-induced Obese Mice

Senna Alata Leaf Extract Restores Insulin Sensitivity In High-fat Diet-induced Obese Mice

Senna alata leaf extract restores insulin sensitivity in high-fat diet-induced obese mice Senna alata (S. alata) has numerous pharmacological activities including anti-lipogenic effect in high-fat diet (HFD)-induced obese mice. The present study investigated the effect of Senna alata (S. alata) leaf extracts on the regulation of abnormal glucose metabolism in HFD-induced obese mice. Male ICR mice were induced to become obese by being fed a HFD (45kcal% lard fat) for 12weeks. During the last 6weeks of diet feeding, the obese mice were treated with the water extract of S. alata leaf at 250 and 500mg/kg/day. After 6weeks of treatment, blood was collected for measuring biochemical parameters. The liver, epididymal fat and skeletal muscle tissues were excised and kept for determining histology and western blot analysis. Treatment with S. alata (250 and 500mg/kg) significantly reduced hyperglycemia, hyperinsulinemia, and hyperleptinemia. The glucose intolerance was improved by S. alata. The elevated monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor- (TNF-) levels in obese mice were reduced in S. alata treatment. The level of serum adiponectin was increased in obese mice treated with S. alata (250 and 500mg/kg). The epididymal fat weight was reduced in S. alata treatment. The enlarged adipocyte size was smaller in obese mice treated with S. alata. In comparison with the obese control mice, the mice treated with S. alata showed a significant reduction of liver glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK) proteins. Moreover, S. alata up-regulated the liver and muscle adenosine monophosphate-activated protein kinase phosphorylation (pAMPK) and muscle glucose transporter 4 (GLUT4). The results indicate that the restoration of imp 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 >>

High Fat Diet Induced Insulin Resistance And Elevated Retinol Binding Protein 4 In Female Rats; Treatment And Protection With Berberis Vulgaris Extract And Vitamin A

High Fat Diet Induced Insulin Resistance And Elevated Retinol Binding Protein 4 In Female Rats; Treatment And Protection With Berberis Vulgaris Extract And Vitamin A

Pak. J. Pharm. Sci., Vol.26, No.6, November 2013, pp.1189-1195 1189 High fat diet induced insulin resistance and elevated retinol binding protein 4 in female rats; treatment and protection with Berberis Mohamed Mohammed El-Sayed1, Doaa Ahmad Ghareeb1*, Heba Allah Talat1 1Biochemistry Department, Faculty of Science, Alexandria University, Alexandria, Egypt 2Protein Research Department, Institute of Genetic Engineering and Biotechnology (GEBRI), SRTA City, Borg Al-Arab, Alexandria University, Alexandria, Egypt Abstract: This research was conducted to investigate two main aims; the first aim was to find if there is a relationship between insulin resistance (IR) and retinol binding protein 4 (RBP4). The second aim was to use berberis vulgaris extract and vitamin A as protective and/or curative agents against insulin resistance. IR was developed by feeding the female rats a high fat diet (HFD) for six weeks then treating or protecting them with b. vulgaris extract (0.2 g/Kg body weight) or vitamin A (12.8g/Kg/day) for two weeks. Results: HFD intake elevated insulin level and RBP4 expression that associated with hyperglycemia and hyperlipidemia. Co-administration of vitamin A and B. vulgaris extracts reduced blood glucose level, insulin, body weight and RBP4 expression before, during and after HFD. Furthermore, vitamin A reduced the blood glucose, triglycerides (TG) and cholesterol levels. IR syndrome associated with the RBP 4 alteration that gives high indication about the role of RBP4 expression in the IR progression and development. Furthermore, the treatment with vitamin A and/or b. vulgaris alleviated the IR syndrome through the action on RBP4 and Insulin secretion. On the other hand, vitamin A must be avoided for the predisposed IR and prediabetic patients. Keywords: I 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 >>

Klf15 Knockout Mice Are Protected Against High-fat Diet Induced Insulin Resistance

Klf15 Knockout Mice Are Protected Against High-fat Diet Induced Insulin Resistance

KLF15 Knockout Mice are Protected Against High-Fat Diet Induced Insulin Resistance The Kruppel-like transcription The Kruppel-like transcription factor KLF15 has been shown to play an important role in the regulation of glucose homeostasis under normal physiological conditions. Our previous reports indicate that mice with a targeted deletion of KLF15 (KLF15-/- mice) exhibit lower fed glucose levels compared to wild-type (WT) mice and hypoglycemia after an overnight fast. Here we investigate the metabolic response of KLF15-/- mice in diet-induced obesity. KLF15-/- mice and WT littermates were fed a high-fat diet (60% fat by calories) for 2 months starting at age 13 weeks. In response to high-fat feeding, both WT and KLF15-/- mice became obese. Daily food intake was increased by ~20% in KLF15-/- mice (p<0.05), but there was no significant difference in the total amount of weight gained between the groups. After 3 weeks of high-fat feeding, KLF15-/- mice showed significantly lower glucose levels (4-hr fasted state) compared to WT mice (WT = 1958 mg/dL, KLF15-/- = 1557 mg/dL; p<0.01). Intraperitoneal glucose tolerance tests were performed at the end of the 2 month period. The results indicate substantially improved glucose tolerance in fat fed KFL15-/- mice compared to fat fed WT mice as indicated by significantly reduced area under the curve of glucose clearance in KFL15-/- mice (WT = 28530 2958 mg/dl*min, KLF15-/- = 11370 1516 mg/dL*min; p<0.001). These results demonstrate that homozygous deletion of KLF15 improves insulin sensitivity in high-fat fed mice, and our findings suggest an important role of KLF15 in the development of obesity-associated insulin resistance. JULIANO SARTORETTO, THOMAS MICHEL, SUSAN GRAY, Boston, MA 1305-P Boston, MA Insulin Action - Metabolism Continue reading >>

Osteopontin Knockout Abates High Fat Diet-induced Insulin Resistance And Adipose Tissue Inflammation

Osteopontin Knockout Abates High Fat Diet-induced Insulin Resistance And Adipose Tissue Inflammation

Osteopontin knockout abates high fat diet-induced insulin resistance and adipose tissue inflammation In recent years type 2 diabetes has been shown to consist of not only insulin resistance of insulin target tissues (muscle, adipose tissue, and liver) but inflammation of adipose tissue as well. This inflammatory state is characterized by increased macrophage infiltration and pro -inflammatory cytokine expression. Given the known pro- inflammatory roles of osteopontin in many pathological states in addition to its cell migration enhancing properties, osteopontin was examined for its effect on diet-induced obesity. Osteopontin knockout mice exhibited increased liver insulin sensitivity by hyperinsulinemic euglycemic clamp after two and 16 weeks on high fat diet compared to the wild type mice. Increased muscle insulin sensitivity was also observable after two weeks on diet by clamp in the knockout mice. Enhanced insulin signaling in muscle, adipose tissue, and liver, assessed by Akt phosphorylation, was also observed in the osteopontin knockout mice versus the wild type mice after high fat feeding, indicating attenuated insulin resistance. Osteopontin knockout mice also showed diminished adipose tissue hypertrophy, triple-positive pro-inflammatory cell infiltration into adipose tissue, and inflammatory cytokine expression, indicating less inflammation of the adipose tissue after short-term high fat diet. Total osteopontin expression as well as differential isomeric expression of it in the adipose tissue was observed to increase after high-fat diet in wild type mice, further implicating its role in inflammation of the adipose tissue. Osteopontin appears to mediate the effects of short- and long-term diet-induced obesity in a cytokine- like manner, leading to localized infl 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 >>

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 >>

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 >>

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 >>

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

Increased oxidative stress precedes the onset of high-fat dietinduced insulin resistance and obesity 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 1c-related fatty acid synthesis and peroxisome proliferator-activated receptor alpha-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-alpha and free fatty acids in the plasma and liver. The ROS may be an initial key event triggering HFD-induced insulin resistance. 2018 Digital Science & Research Solutions, Inc. All Rights Reserved | About us Privacy policy Legal terms VPAT Citation Count is the number of times that this paper has been cited by other published papers in the database. The Altmetric Attention Score is a weighted count of all of the online attention Altmetric have found for an individual research output. This includes mentions in public policy documents and references in Wikipedia, the mainstream news, soc 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 >>

Consumption Of A Mango Fruit Powder Protects Mice From High-fat Induced Insulin Resistance And Hepatic Fat Accumulation

Consumption Of A Mango Fruit Powder Protects Mice From High-fat Induced Insulin Resistance And Hepatic Fat Accumulation

Abstract Background/Aims: The aim of this study was to gain more insight into the beneficial effects of mango fruit powder on the early metabolic adverse effects of a high-fat diet. Methods: The progressive dose-response effects of mango fruit powder on body composition, circulating parameters, and the expression of genes related to fatty acid oxidation and insulin sensitivity in key tissues were studied in mice fed a moderate (45%) high-fat diet. Results: Findings suggest that mango fruit powder exerts physiological protective effects in the initial steps of insulin resistance and hepatic lipid accumulation induced by a high-fat diet in mice. Moreover, AMPK and SIRT1 appear as key regulators of the observed improvement in fatty acid oxidation capacity, as well as of the improved insulin sensitivity and the increased glucose uptake and metabolism through the glycolytic pathway capacity in liver and skeletal muscle. Conclusion: In summary, this study provides evidence that the functional food ingredient (CarelessTM) from mango fruit prevents early metabolic alterations caused by a high-fat diet in the initial stages of the metabolic syndrome. © 2017 The Author(s). Published by S. Karger AG, Basel Introduction Dysregulated glucose and lipid metabolism and, thus, energy homeostasis are early events in the development of insulin resistance, which in turn may lead to obesity and diabetes mellitus type 2. The overall prevalence of insulin resistance in developed societies is high, with 11.5-14.0% of the European population [1], 20% of adults in Japan [2], and nearly 30% of adult Americans [3] being afflicted. The insensitivity of peripheral tissues to the effects of insulin starts when the nutrient storage metabolic pathways are exposed to persistent energy excess, surpassin Continue reading >>

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