title: Differential proinflammatory and oxidative stress response and vulnerability to metabolic syndrome in habitual high-fat young male consumers putatively predisposed by their genetic background.
abstract: The current nutritional habits and lifestyles of modern societies favor energy overloads and a diminished physical activity, which may produce serious clinical disturbances and excessive weight gain. In order to investigate the mechanisms by which the environmental factors interact with molecular mechanisms in obesity, a pathway analysis was performed to identify genes differentially expressed in subcutaneous abdominal adipose tissue (SCAAT) from obese compared to lean male (21-35 year-old) subjects living in similar obesogenic conditions: habitual high fat dietary intake and moderate physical activity. Genes involved in inflammation (ALCAM, CTSB, C1S, YKL-40, MIF, SAA2), extracellular matrix remodeling (MMP9, PALLD), angiogenesis (EGFL6, leptin) and oxidative stress (AKR1C3, UCHL1, HSPB7 and NQO1) were upregulated; whereas apoptosis, signal transcription (CITED 2 and NR3C1), cell control and cell cycle-related genes were downregulated. Interestingly, the expression of some of these genes (C1S, SAA2, ALCAM, CTSB, YKL-40 and tenomodulin) was found to be associated with some relevant metabolic syndrome features. The obese group showed a general upregulation in the expression of inflammatory, oxidative stress, extracellular remodeling and angiogenic genes compared to lean subjects, suggesting that a given genetic background in an obesogenic environment could underlie the resistance to gaining weight and obesity-associated manifestations.
authors: Department of Nutrition, Food Sciences and Physiology, University of Navarra, 31008 Pamplona, Spain. pgonmun@unav.es
authors: Pedro
authors: P
authors: González-Muniesa
authors: María Pilar
authors: MP
authors: Marrades
authors: José Alfredo
authors: JA
authors: Martínez
authors: María Jesús
authors: MJ
authors: Moreno-Aliaga
mesh_terms: D000328:Adult; D002135:Calcium-Binding Proteins; D015815:Cell Adhesion Molecules; D006801:Humans; D007249:Inflammation / Q000235:genetics; D020738:Leptin / Q000235:genetics; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000235:genetics; D008562:Membrane Glycoproteins / Q000235:genetics; D024821:Metabolic Syndrome / Q000235:genetics / Q000276:immunology* / Q000378:metabolism*; D009765:Obesity / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D018384:Oxidative Stress / Q000235:genetics / Q000276:immunology*; D011965:Receptors, Glucocorticoid / Q000235:genetics; D050151:Subcutaneous Fat / Q000378:metabolism; D043222:Ubiquitin Thiolesterase / Q000235:genetics; D055815:Young Adult
chemical_list: D002135:Calcium-Binding Proteins; D015815:Cell Adhesion Molecules; C403518:EGFL6 protein, human; D020738:Leptin; D008562:Membrane Glycoproteins; C497713:NR3C1 protein, human; D011965:Receptors, Glucocorticoid; C482860:UCHL1 protein, human; D043222:Ubiquitin Thiolesterase; D020780:Matrix Metalloproteinase 9
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