title: Dietary cocoa ameliorates obesity-related inflammation in high fat-fed mice.
abstract: OBJECTIVE
  To investigate the effect of cocoa powder supplementation on obesity-related inflammation in high fat (HF)-fed obese mice.
  
  
  METHODS
  Male C57BL/6J (n = 126) were fed with either low-fat (LF, 10 % kcal from fat) or HF (60 % kcal from fat) diet for 18 weeks. After 8 weeks, mice from HF group were randomized to HF diet or HF diet supplemented with 8 % cocoa powder (HF-HFC group) for 10 weeks. Blood and tissue samples were collected for biochemical analyses.
  
  
  RESULTS
  Cocoa powder supplementation significantly reduced the rate of body weight gain (15.8 %) and increased fecal lipid content (55.2 %) compared to HF-fed control mice. Further, cocoa supplementation attenuated insulin resistance, as indicated by improved HOMA-IR, and reduced the severity of obesity-related fatty liver disease (decreased plasma alanine aminotransferase and liver triglyceride) compared to HF group. Cocoa supplementation also significantly decreased plasma levels of the pro-inflammatory mediators interleukin-6 (IL-6, 30.4 %), monocyte chemoattractant protein-1 (MCP-1, 25.2 %), and increased adiponectin (33.7 %) compared to HF-fed mice. Expression of pro-inflammatory genes (Il6, Il12b, Nos2, and Emr1) in the stromal vascular fraction (SVF) of the epididymal white adipose tissue (WAT) was significantly reduced (37-56 %) in the cocoa-supplemented mice.
  
  
  CONCLUSIONS
  Dietary supplementation with cocoa ameliorates obesity-related inflammation, insulin resistance, and fatty liver disease in HF-fed obese mice, principally through the down-regulation of pro-inflammatory gene expression in WAT. These effects appear to be mediated in part by a modulation of dietary fat absorption and inhibition of macrophage infiltration in WAT.
authors.affiliation: Center of Excellence for Plant and Mushroom Foods and Health, Department of Food Science, The Pennsylvania State University, 332 Food Science Building, University Park, PA, 16802, USA.
authors.forename: Yeyi
authors.initials: Y
authors.lastname: Gu
authors.forename: Shan
authors.initials: S
authors.lastname: Yu
authors.forename: Joshua D
authors.initials: JD
authors.lastname: Lambert
mesh_terms: D052242:Adiponectin / Q000097:blood; D052436:Adipose Tissue, White / Q000378:metabolism; D000818:Animals; D002099:Cacao / Q000737:chemistry*; D002135:Calcium-Binding Proteins; D018932:Chemokine CCL2 / Q000097:blood; D059305:Diet, High-Fat; D002149:Energy Intake; D005234:Fatty Liver / Q000097:blood / Q000150:complications*; D007249:Inflammation / Q000097:blood / Q000150:complications*; D007333:Insulin Resistance; D053762:Interleukin-12 Subunit p40 / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000097:blood / Q000235:genetics; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008820:Mice, Obese; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D009765:Obesity / Q000097:blood / Q000150:complications*; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled; D014280:Triglycerides / Q000378:metabolism; D015430:Weight Gain
chemical_list: C000634132:Adgre1 protein, mouse; D052242:Adiponectin; D002135:Calcium-Binding Proteins; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D053762:Interleukin-12 Subunit p40; D015850:Interleukin-6; D011956:Receptors, Cell Surface; D043562:Receptors, G-Protein-Coupled; D014280:Triglycerides; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse