How fatty acids and common genetic variants together affect the inflammation of adipose tissue

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Abstract

Adipose tissue (AT) expansion is associated with the recruitment of additional macrophages and a proinflammatory adipokine profile. The inflammatory status of AT is an important determinant of the metabolic and pathologic consequences of obesity and the risk of comorbidities such as type 2 diabetes and nonalcoholic fatty liver disease. It has more recently also been linked to dementia and accelerated brain ageing. Given that fatty acids regulate cellular inflammation through their impact on the eicosanoid profile and on adipokine expression, it is likely that habitual fatty acid intake and AT fatty acid status, is important in regulating AT inflammation. Furthermore, although as yet poorly researched and understood, common variants in inflammatory genes and in their receptors and regulators may influence their production and overall AT function. In an era where population weight reduction strategies have had limited success, an understanding of AT inflammation and its regulation by dietary strategies aimed at resulting in a ‘metabolically healthy obese phenotype,’ is of wide public health relevance.
Original languageEnglish
Article number411
JournalCurrent Cardiovascular Risk Reports
Volume8
Early online date27 Sep 2014
DOIs
Publication statusPublished - Nov 2014

Keywords

  • Obesity
  • BMI
  • Waist
  • Hypertrophy
  • Genotype
  • GWAS
  • Insulin sensitivity
  • Inflammation
  • Macrophages
  • Cytokines
  • Adipokines
  • Adiponectin
  • TNFα
  • IL-6
  • Apolipoprotein E
  • n-3 PUFA
  • Saturated fatty acids

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