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Polyphenol-rich blackcurrant extract prevents inflammation in diet-induced obese mice

J Nutr Biochem. 2014 Oct;25(10):1019-25. doi: 10.1016/j.jnutbio.2014.05.008. Epub 2014 Jun 13.

Abstract

Obesity is closely associated with chronic, low-grade inflammation. We investigated if polyphenol-rich blackcurrant extract (BCE) can prevent inflammation in vivo. Male C57BL/6J mice were fed a modified AIN-93M control diet containing high fat/high cholesterol (16% fat, 0.25% cholesterol by weight) or the control diet supplemented with 0.1% BCE (wt/wt) for 12 weeks. In BCE-fed mice, the percentage of body weight and adipocyte size of the epididymal fat were significantly lower than those of control mice. There were fewer crown-like structures (CLS) with concomitant decreases in F4/80, cluster of differentiation 68 and inhibitor of nuclear factor κB kinase ε (IKKε) mRNA in the epididymal adipose of BCE-fed mice. F4/80 and IKKε mRNA levels were positively correlated with CLS number. In the skeletal muscle of mice fed with BCE, mRNA expression of genes involved in energy expenditure and mitochondrial biogenesis, including PPARα, PPARδ, UCP-2, UCP-3 and mitochondrial transcription factor A, were significantly increased. When splenocytes from BCE-fed mice were stimulated by lipopolysaccharides, tumor necrosis factor α and interleukin-1β mRNA were significantly lower than control splenocytes. Together, the results suggest that BCE supplementation decreases obesity-induced inflammation in adipose tissue and splenocytes, at least in part, by modulating energy metabolism in skeletal muscle.

Keywords: Anthocyanins; Blackcurrant; Crown-like structure; Inflammation; Macrophage infiltration; Obesity.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Adipocytes / drug effects
  • Adipocytes / metabolism
  • Adipose Tissue / drug effects
  • Adipose Tissue / metabolism
  • Animals
  • Anthocyanins / analysis
  • Anthocyanins / pharmacology
  • Antigens, CD / genetics
  • Antigens, CD / metabolism
  • Antigens, Differentiation, Myelomonocytic / genetics
  • Antigens, Differentiation, Myelomonocytic / metabolism
  • Body Weight
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism
  • Diet, High-Fat / adverse effects
  • Epigenetic Repression
  • I-kappa B Kinase / genetics
  • I-kappa B Kinase / metabolism
  • Inflammation / drug therapy
  • Inflammation / etiology
  • Inflammation / prevention & control*
  • Interleukin-1beta / metabolism
  • Ion Channels / genetics
  • Ion Channels / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mitochondrial Proteins / genetics
  • Mitochondrial Proteins / metabolism
  • Mitochondrial Turnover
  • Muscle, Skeletal / drug effects
  • Muscle, Skeletal / metabolism
  • Obesity / complications
  • Obesity / drug therapy
  • PPAR alpha / genetics
  • PPAR alpha / metabolism
  • PPAR gamma / genetics
  • PPAR gamma / metabolism
  • Plant Extracts / analysis
  • Plant Extracts / pharmacology*
  • Polyphenols / analysis
  • Polyphenols / pharmacology*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Ribes / chemistry*
  • Spleen / cytology
  • Spleen / drug effects
  • Spleen / metabolism
  • Transcription Factors / genetics
  • Transcription Factors / metabolism
  • Tumor Necrosis Factor-alpha / metabolism
  • Uncoupling Protein 2
  • Uncoupling Protein 3

Substances

  • Anthocyanins
  • Antigens, CD
  • Antigens, Differentiation, Myelomonocytic
  • CD68 antigen, human
  • DNA-Binding Proteins
  • Interleukin-1beta
  • Ion Channels
  • Mitochondrial Proteins
  • PPAR alpha
  • PPAR gamma
  • Plant Extracts
  • Polyphenols
  • RNA, Messenger
  • Transcription Factors
  • Tumor Necrosis Factor-alpha
  • UCP2 protein, human
  • UCP3 protein, human
  • Ucp2 protein, mouse
  • Ucp3 protein, mouse
  • Uncoupling Protein 2
  • Uncoupling Protein 3
  • mitochondrial transcription factor A
  • I-kappa B Kinase