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Energy restriction with high‐protein diets decreases visceral fat mass but not fasting and postprandial inflammation in overweight insulin‐resistant rats
Author(s) -
Mariotti Francois,
Xu Liping,
Mathé Véronique,
Brunsard Julie,
Magné Joelle,
Bos Cécile,
Tomé Daniel,
Gaudichon Claire,
Huneau JeanFrancois
Publication year - 2009
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.23.1_supplement.910.9
Subject(s) - postprandial , medicine , endocrinology , overweight , meal , intermittent fasting , insulin , hfr cell , insulin resistance , obesity , inflammation , biology , biochemistry , escherichia coli , gene
Visceral obesity may worsen the low‐grade postprandial inflammatory response to a high‐fat meal. To test this hypothesis, we studied the effects of energy restriction in rats with diet‐induced overweight. Overweight rats were given free‐access to a high‐fat diet (HF), or restricted to 60% of the spontaneous intake of HF rats, with either the same diet (HFR) or protein‐rich diets (HPR) for 5 weeks. Before and at the end of this period, rats were administered a high‐fat meal and plasma insulin, triglycerides and cytokines were monitored after meal. Rats were killed at the end of the experiment and the epididymal fat pads were weighed. At the end of the experiment, the weights of the restricted rat were similar between HFR and HPR groups and 19%‐lower than in HF rats. However, the epididymal fat masses were slightly but significantly lower in HPR rats than in HFR and HF rats (14.5±0.6, 17.4±1.2 and 24.0±2.3 g, respectively). Fasting insulin did not change in restricted rats, while almost doubling in HF rats. At the end of the experiment, fasting and postprandial increases in IL‐1β, IL‐6, MCP‐1 and PAI‐1 did not differ between groups. Altogether, these results suggest that decreasing visceral adiposity in insulin‐resistant overweight rats does not impact fasting and postprandial low‐grade inflammation.