Premium
Effects of Pomegranate Extract on High Fat/High Sucrose Diet induced Obesity are Dependent on the Intestinal Formation of Urolithin A
Author(s) -
Yang Jieping,
Henning Susanne M,
Lee Rupo,
Hsu Mark,
Grojean Emma M,
Ly Austin,
Heber David,
Li Zhaoping
Publication year - 2016
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.30.1_supplement.691.28
Subject(s) - ellagic acid , cecum , food science , sucrose , chemistry , corn oil , adipose tissue , gut flora , gastrointestinal tract , obesity , biology , biochemistry , medicine , polyphenol , endocrinology , antioxidant
Recent studies strongly suggest the association of gut microbiota and obesity related diseases. Published data from a mouse study demonstrated that pomegranate extract (PomX) administration increased cecum Bifidobacteria , decreased inflammation and counteracted the HF‐induced expression of inflammatory markers both in colon and visceral adipose tissue. The major phytochemicals in PomX are ellagitannins (ETs), which are not absorbed in the small intestine. ETs are hydrolyzed to ellagic acid (EA) in the stomach and further metabolized to urolithin A (UA) by bacteria in the gastrointestinal tract. Inter‐individual differences in the production of UA from PomX were previously reported in humans. About 30% of individuals cannot produce UA when consuming POM.The aim of the present study was to investigateand link the potential effects of PomX on metabolic abnormalities of mice fed with HF/HS diet to intestinal UA formation. C57BL/6 male mice were randomly assigned to two treatment groups: control high fat /high sucrose [HF/HS (32% kcal from butter fat and corn oil, 25% kcal from sucrose)], or a HF/HS diet supplemented with 0.25% PomX for 4 weeks. In the mice receiving 0.25% PomX diet, stool samples were collected and analyzed by high performance liquid chromatography for UA production. We observed two distinct groups: UA producer (Producer) and UA non‐producer (Non‐P). All observations are in comparison to the HF/HS fed control mice. About 40% of mice fed the 0.25% PomX diet did not produce UA during the 4 week feeding period. The Non‐Ps showed significantly higher concentration of EA in blood and feces compared to producers. PomX administration significantly decreased liver lipid content and serum endotoxin in both producers and Non‐Ps associated with increase of hepatic AMPK phosporylation. However epididymal and mesenteric fat depots were only significantly increased by PomX consumption in producers meanwhile the cecum Bifidobacterium and Lactobacillus abundance only increased in Non‐Ps. In both Non‐Ps and producers PomX consumption did not significantly modify body weight gain, subcutaneous fat, Bacteroidetes / Firmicutes ratio and Akkermansia abundance. In summary, mice lacking UA production show higher EA concentrations in blood and feces while UA producers showed higher UA in blood and feces. Depending on their capacity to form UA we observed different effects of PomX diet on Bifidobacterium and Lactobacillus abundance and fat disposition using this HF/HS diet induced obesity mouse model. Support or Funding Information Supported by departmental funds from the Center for Human Nutrition, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles.