Please use this identifier to cite or link to this item: http://hdl.handle.net/10668/768
Título : Progression from high insulin resistance to type 2 diabetes does not entail additional visceral adipose tissue inflammation.
Autor : Barbarroja Puerto, Nuria
López-Pedrera, Chary
Garrido-Sánchez, Lourdes
Mayas Torres, María Dolores
Oliva-Olivera, Wilfredo
Bernal-López, María Rosa
El Bekay, Rajaa
Tinahones Madueño, Francisco José
Filiación: [Barbarroja Puerto,N; Oliva-Olivera,W; Bernal-López,MR; El Bekay,R; Tinahones Madueño,FJ] Servicio de Endocrinología y Nutrición, Hospital Universitario Virgen de la Victoria, Málaga, Spain. [Barbarroja Puerto,N; Oliva-Olivera,W; Bernal-López,MR; El Bekay,R; Tinahones Madueño,FJ] Fundación IMABIS, Málaga, Spain. [Barbarroja Puerto,N; Oliva-Olivera,W; Bernal-López,MR; El Bekay,R; Tinahones Madueño,FJ] CIBER Fisiopatología de la Obesidad y Nutrición CB06/03, Instituto de Salud Carlos III, Madrid, Spain. [López-Pedrera,C] Unidad de Investigación, Hospital Reina Sofía-IMIBIC, Córdoba, Spain [Garrido-Sánchez,L] CIBERDEM, Hospital Universitari de Tarragona Joan XXIII, IISPV, Universitat Rovira i Virgili, Tarragona, Spain. [Mayas Torres,MD] Área de Fisiología, Universidad de Jaén, Spain.
Palabras clave : Inflamación
Resistencia a la Insulina
Obesidad Mórbida
Diabetes Mellitus Tipo 2
Grasa Intraabdominal
FN-kappa B
Interleucina-1beta
Interleucina-6
Lípidos
ARN Mensajero
Proteína Quinasa 1 Activada por Mitógenos
Quinasa Activada por Mitógeno 3
Quinasas MAP Reguladas por Señal Extracelular
Factor de Transcripción STAT3
Factor de Necrosis Tumoral alfa
Humanos
MeSH: Medical Subject Headings::Diseases::Pathological Conditions, Signs and Symptoms::Pathologic Processes::Inflammation
Medical Subject Headings::Diseases::Nutritional and Metabolic Diseases::Metabolic Diseases::Glucose Metabolism Disorders::Hyperinsulinism::Insulin Resistance
Medical Subject Headings::Diseases::Nutritional and Metabolic Diseases::Nutrition Disorders::Overnutrition::Obesity::Obesity, Morbid
Medical Subject Headings::Diseases::Nutritional and Metabolic Diseases::Metabolic Diseases::Glucose Metabolism Disorders::Diabetes Mellitus::Diabetes Mellitus, Type 2
Medical Subject Headings::Anatomy::Tissues::Connective Tissue::Adipose Tissue::Adipose Tissue, White::Abdominal Fat::Intra-Abdominal Fat
Medical Subject Headings::Chemicals and Drugs::Amino Acids, Peptides, and Proteins::Proteins::DNA-Binding Proteins::NF-kappa B
Medical Subject Headings::Chemicals and Drugs::Amino Acids, Peptides, and Proteins::Peptides::Intercellular Signaling Peptides and Proteins::Cytokines::Interleukins::Interleukin-1::Interleukin-1beta
Medical Subject Headings::Chemicals and Drugs::Amino Acids, Peptides, and Proteins::Peptides::Intercellular Signaling Peptides and Proteins::Cytokines::Interleukins::Interleukin-6
Medical Subject Headings::Chemicals and Drugs::Lipids
Medical Subject Headings::Chemicals and Drugs::Nucleic Acids, Nucleotides, and Nucleosides::Nucleic Acids::RNA::RNA, Messenger
Medical Subject Headings::Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Transferases::Phosphotransferases::Phosphotransferases (Alcohol Group Acceptor)::Protein Kinases::Protein-Serine-Threonine Kinases::Proline-Directed Protein Kinases::Mitogen-Activated Protein Kinases::Extracellular Signal-Regulated MAP Kinases::Mitogen-Activated Protein Kinase 1
Medical Subject Headings::Chemicals and Drugs::Amino Acids, Peptides, and Proteins::Peptides::Intracellular Signaling Peptides and Proteins::Mitogen-Activated Protein Kinases::Extracellular Signal-Regulated MAP Kinases::Mitogen-Activated Protein Kinase 3
Medical Subject Headings::Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Transferases::Phosphotransferases::Phosphotransferases (Alcohol Group Acceptor)::Protein Kinases::Protein-Serine-Threonine Kinases::Mitogen-Activated Protein Kinases::Extracellular Signal-Regulated MAP Kinases
Medical Subject Headings::Chemicals and Drugs::Amino Acids, Peptides, and Proteins::Peptides::Intracellular Signaling Peptides and Proteins::Adaptor Proteins, Signal Transducing::STAT Transcription Factors::STAT3 Transcription Factor
Medical Subject Headings::Chemicals and Drugs::Amino Acids, Peptides, and Proteins::Peptides::Intercellular Signaling Peptides and Proteins::Cytokines::Monokines::Tumor Necrosis Factor-alpha
Medical Subject Headings::Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans
Fecha de publicación : 24-Oct-2012
Editorial : Public Library of Science
Cita Bibliográfica: Barbarroja Puerto N, López-Pedrera C, Garrido-Sánchez L, Mayas Torres MD, Oliva-Olivera W, Bernal-López MR, et al. Progression from high insulin resistance to type 2 diabetes does not entail additional visceral adipose tissue inflammation. PLoS ONE. 2012; 7(10):e48155
Abstract: Obesity is associated with a low-grade chronic inflammation state. As a consequence, adipose tissue expresses pro-inflammatory cytokines that propagate inflammatory responses systemically elsewhere, promoting whole-body insulin resistance and consequential islet β-cell exhaustation. Thus, insulin resistance is considered the early stage of type 2 diabetes. However, there is evidence of obese individuals that never develop diabetes indicating that the mechanisms governing the association between the increase of inflammatory factors and type 2 diabetes are much more complex and deserve further investigation. We studied for the first time the differences in insulin signalling and inflammatory pathways in blood and visceral adipose tissue (VAT) of 20 lean healthy donors and 40 equal morbidly obese (MO) patients classified in high insulin resistance (high IR) degree and diabetes state. We studied the changes in proinflammatory markers and lipid content from serum; macrophage infiltration, mRNA expression of inflammatory cytokines and transcription factors, activation of kinases involved in inflammation and expression of insulin signalling molecules in VAT. VAT comparison of these experimental groups revealed that type 2 diabetic-MO subjects exhibit the same pro-inflammatory profile than the high IR-MO patients, characterized by elevated levels of IL-1β, IL-6, TNFα, JNK1/2, ERK1/2, STAT3 and NFκB. Our work rules out the assumption that the inflammation should be increased in obese people with type 2 diabetes compared to high IR obese. These findings indicate that some mechanisms, other than systemic and VAT inflammation must be involved in the development of type 2 diabetes in obesity.
Descripción : Journal Article;
URI: http://hdl.handle.net/10668/768
Versión del editor : http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0048155
DOI: 10.1371/journal.pone.0048155
ISSN : 1932-6203 (Online)
Appears in Collections:01- Artículos - Hospital Virgen de la Victoria
01- Artículos - IMIBIC. Instituto Maimónides de Investigación Biomédica de Córdoba
01- Artículos - Hospital Reina Sofía

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