Premium
Cranberry Extract Ameliorates Obesity‐Related Liver Inflammation via the Toll‐Like Receptor 4 Pathway
Author(s) -
Glisan Shan,
Lambert Joshua
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.118.3
Subject(s) - medicine , endocrinology , nonalcoholic fatty liver disease , inflammation , fatty liver , cirrhosis , liver x receptor alpha , triglyceride , tumor necrosis factor alpha , chemokine , adipose tissue , chemistry , nuclear receptor , cholesterol , biochemistry , disease , transcription factor , gene
Obesity is commonly associated with an increase in hepatic triglycerides, known as nonalcoholic fatty liver disease (NAFLD). NAFLD may progress into nonalcoholic steatohepatitis (NASH), which includes an inflammatory component, and eventually cirrhosis. Polyphenols, such as those found in cranberries, have been shown to have antioxidant and anti‐inflammatory properties. The objective of this study was to determine the effect of cranberry extract (CBE) on NASH in an obese mouse model. C57bl/6J mice fed either 60%kcal from fat diet (HF, n=48) or 10%kcal from fat diet (LF, n=12). After 11 weeks, 24 mice from the HF group were switched to HF diet supplemented with 0.8% CBE. After an additional 10 weeks, mice were euthanized and markers of obesity and NAFLD were examined. Body weight, relative liver weight, and liver triglyceride concentrations were not affected by CBE supplementation. CBE supplementation did significantly decrease circulating alanine aminotransferase levels compared to the HF group, indicating a decrease in liver injury. Supplementation with CBE resulted in a decrease in hepatic toll‐like receptor 4 gene expression (63%) and hepatic nuclear factor (NF)‐κB gene expression (24%) compared to the HF group. Hepatic expression of tumor necrosis factor alpha, a pro‐inflammatory cytokine gene regulated by NF‐κB, and C‐C chemokine receptor 2 (CCR2), a receptor for monocyte chemoattractant protein‐1 was significantly decreased by CBE supplementation compared to HF mice. In conclusion, CBE may mitigate obesity‐related hepatic inflammation and liver damage; however, additional experiments are needed to better understand the underlying mechanisms of action.