Dietary cocoa ameliorates obesity-related inflammation in high fat-fed mice

Yeyi Gu, Shan Yu, Joshua D. Lambert

Research output: Contribution to journalArticle

51 Citations (Scopus)

Abstract

Purpose: 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.

Original languageEnglish (US)
Pages (from-to)149-158
Number of pages10
JournalEuropean Journal of Nutrition
Volume53
Issue number1
DOIs
StatePublished - Feb 1 2014

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Obesity
Fats
Inflammation
White Adipose Tissue
Obese Mice
High Fat Diet
Fatty Liver
Insulin Resistance
Liver Diseases
Interleukin-6
Chemokine CCL2
Dietary Fats
Adiponectin
Dietary Supplements
Alanine Transaminase
Weight Gain
Blood Vessels
Triglycerides
Down-Regulation
Macrophages

All Science Journal Classification (ASJC) codes

  • Medicine (miscellaneous)
  • Nutrition and Dietetics

Cite this

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title = "Dietary cocoa ameliorates obesity-related inflammation in high fat-fed mice",
abstract = "Purpose: 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.",
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Dietary cocoa ameliorates obesity-related inflammation in high fat-fed mice. / Gu, Yeyi; Yu, Shan; Lambert, Joshua D.

In: European Journal of Nutrition, Vol. 53, No. 1, 01.02.2014, p. 149-158.

Research output: Contribution to journalArticle

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T1 - Dietary cocoa ameliorates obesity-related inflammation in high fat-fed mice

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AU - Yu, Shan

AU - Lambert, Joshua D.

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N2 - Purpose: 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.

AB - Purpose: 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.

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