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A safflower oil based high‐fat/high‐sucrose diet modulates the gut microbiota and liver phospholipid profiles associated with early glucose intolerance in the absence of tissue inflammation
Author(s) -
DanneskioldSamsøe Niels Banhos,
Andersen Daniel,
Radulescu Ilinca Daria,
NormannHansen Ann,
Brejnrod Asker,
Kragh Marie,
Madsen Tobias,
Nielsen Christian,
Josefsen Knud,
Fretté Xavier,
Fjære Even,
Madsen Lise,
Hellgren Lars I.,
Brix Susanne,
Kristiansen Karsten
Publication year - 2017
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201600528
Subject(s) - endocrinology , gut flora , medicine , polyunsaturated fatty acid , biology , inflammation , arachidonic acid , immune system , linoleic acid , fatty acid , biochemistry , immunology , enzyme
Scope Omega‐6 ( n ‐6) PUFA‐rich diets are generally considered obesogenic in rodents. Here, we examined how long‐term intake of a high‐fat/high‐sucrose (HF/HS) diet based on safflower oil affected metabolism, inflammation, and gut microbiota composition. Methods and results We fed male C57BL/6J mice a HF/HS diet based on safflower oil—rich in n ‐6 PUFAs—or a low‐fat/low‐sucrose diet for 40 wk. Compared to the low‐fat/low‐sucrose diet, intake of the safflower‐based HF/HS diet only led to moderate weight gain, while glucose intolerance developed at week 5 prior to signs of inflammation, but concurrent with increased levels of linoleic acid and arachidonic acid in hepatic phospholipids. Intake of the HF/HS diet resulted in early changes in the gut microbiota, including an increased abundance of Blautia , while late changes coincided with altered inflammatory profiles and increased fasting plasma insulin. Analysis of immune cells in visceral fat and liver revealed no differences between diets before week 40, where the number of immune cells decreased in the liver of HF/HS‐fed mice. Conclusion We suggest that a diet‐dependent increase in the n ‐6 to omega‐3 ( n ‐3) PUFA ratio in hepatic phospholipids together with gut microbiota changes contributed to early development of glucose intolerance without signs of inflammation.