Differential proinflammatory and oxidative stress response and vulnerability to metabolic syndrome in habitual high-fat young male consumers putatively predisposed by their genetic background

Int J Mol Sci. 2013 Aug 22;14(9):17238-55. doi: 10.3390/ijms140917238.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Calcium-Binding Proteins
  • Cell Adhesion Molecules
  • Humans
  • Inflammation / genetics
  • Leptin / genetics
  • Male
  • Matrix Metalloproteinase 9 / genetics
  • Membrane Glycoproteins / genetics
  • Metabolic Syndrome / genetics
  • Metabolic Syndrome / immunology*
  • Metabolic Syndrome / metabolism*
  • Obesity / genetics
  • Obesity / immunology
  • Obesity / metabolism*
  • Oxidative Stress / genetics
  • Oxidative Stress / immunology*
  • Receptors, Glucocorticoid / genetics
  • Subcutaneous Fat / metabolism
  • Ubiquitin Thiolesterase / genetics
  • Young Adult

Substances

  • Calcium-Binding Proteins
  • Cell Adhesion Molecules
  • EGFL6 protein, human
  • Leptin
  • Membrane Glycoproteins
  • NR3C1 protein, human
  • Receptors, Glucocorticoid
  • UCHL1 protein, human
  • Ubiquitin Thiolesterase
  • Matrix Metalloproteinase 9