Black elderberry extract attenuates inflammation and metabolic dysfunction in diet-induced obese mice

• Published in: British journal of nutrition 2015-10, Vol.114 (8), p.1123-1131
• Main Authors: Farrell, Nicholas J., Norris, Gregory H., Ryan, Julia, Porter, Caitlin M., Jiang, Christina, Blesso, Christopher N.
• Format: Article
• Language: English
• Subjects: Adipose tissue; Adipose Tissue - drug effects; Adipose Tissue - metabolism; Animal models; Animals; Berries; Body Weight; Chemokine CCL2 - blood; Diet; Diet, Fat-Restricted; Diet, High-Fat - adverse effects; Dietary Fats - administration & dosage; Dietary Fats - adverse effects; Disease Models, Animal; Dose-Response Relationship, Drug; Histology; Inflammation; Inflammation - drug therapy; Insulin - blood; Insulin Resistance; Interleukin-6 - metabolism; Liver - drug effects; Liver - metabolism; Male; Metabolism; Mice; Mice, Inbred C57BL; Mice, Obese; Molecular Nutrition; Muscle, Skeletal - drug effects; Muscle, Skeletal - metabolism; Obesity; Obesity - drug therapy; Plant Extracts - pharmacology; PPAR gamma - genetics; PPAR gamma - metabolism; RNA, Messenger - genetics; RNA, Messenger - metabolism; Rodents; Sambucus nigra - chemistry; Tumor Necrosis Factor-alpha - blood
• ISSN: 0007-1145; 1475-2662
• DOI: 10.1017/S0007114515002962

Dietary anthocyanins have been shown to reduce inflammation in animal models and may ameliorate obesity-related complications. Black elderberry is one of the richest sources of anthocyanins. We investigated the metabolic effects of anthocyanin-rich black elderberry extract (BEE) in a diet-induced obese C57BL/6J mouse model. Mice were fed either a low-fat diet (n 8), high-fat lard-based diet (HFD; n 16), HFD+0·25 % (w/w) BEE (0·25 %-BEE; n 16) or HFD+1·25 % BEE (1·25 %-BEE; n 16) for 16 weeks. The 0·25 % BEE (0·034 % anthocyanin, w/w) and 1·25 % BEE (0·17 % anthocyanin, w/w) diets corresponded to estimated anthocyanin doses of 20–40 mg and 100–200 mg per kg of body weight, respectively. After 16 weeks, both BEE groups had significantly lower liver weights, serum TAG, homoeostasis model assessment and serum monocyte chemoattractant protein-1 compared with HFD. The 0·25 %-BEE also had lower serum insulin and TNFα compared with HFD. Hepatic fatty acid synthase mRNA was lower in both BEE groups, whereas PPARγ2 mRNA and liver cholesterol were lower in 1·25 %-BEE, suggesting decreased hepatic lipid synthesis. Higher adipose PPARγ mRNA, transforming growth factor β mRNA and adipose tissue histology suggested a pro-fibrogenic phenotype that was less inflammatory in 1·25 %-BEE. Skeletal muscle mRNA expression of the myokine IL-6 was higher in 0·25 %-BEE relative to HFD. These results suggest that BEE may have improved some metabolic disturbances present in this mouse model of obesity by lowering serum TAG, inflammatory markers and insulin resistance.