Dietary cocoa ameliorates obesity-related inflammation in high fat-fed mice
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To investigate the effect of cocoa powder supplementation on obesity-related inflammation in high fat (HF)-fed obese mice.
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.
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.
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.
KeywordsTheobroma cacao Cocoa Polyphenols Inflammation Obesity
Adipose tissue-associated macrophage
Degree of polymerization
High-fat diet supplemented with 8 % cocoa powder
Homeostasis model assessment of insulin resistance
Inducible nitric oxide synthase
Monocyte chemoattractant protein-1
Obesity-related fatty liver disease
Stromal vascular fraction
Tumor necrosis factor-α
White adipose tissue
The authors would like to acknowledge Dr. Sarah Forester, Ms. Sudathip Sae-tan, Ms. Tongtong Xu, Ms. Ling Tao, Mr. Zachary Bitzer, and Ms. Amy Brownschidle for technical assistance.
Conflict of interest
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