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Effect of prenatal and/or postnatal high fat diet on growth, metabolic parameters, blood pressure and motivation in borderline hypertensive rats (BHR)
Author(s) -
Mitra Anaya,
Alvers Kristin,
Crump Erica,
Rowland Neil E.
Publication year - 2008
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.22.1_supplement.882.2
Subject(s) - weaning , cafeteria , offspring , endocrinology , medicine , blood pressure , lactation , obesity , biology , pregnancy , pathology , genetics
The purpose of this study is to determine whether maternal over‐nutrition contributes to obesity, hypertension, and altered glucose handling in rats with a genetic predisposition to mild hypertension. Adult female Wistar rats were maintained on either a high‐fat (HF: 60% lard) or low fat (LF: 10%) diet for approximately 8 weeks, after which they were mated with male spontaneously hypertensive rats (SHR) to yield BHR offspring. Gestating females were maintained on the same diets as prior to impregnation. At parturition, the litters were culled and cross‐fostered either to a dam with either low or high fat diet, so yielding 4 groups for the period of lactation: HF/HF, LF/LF, HF/LF, LF/HF. At weaning, half the females from the litters were fed Purina chow while the other half were placed on a varied HF cafeteria diet for the entire duration of the experiments. At PD 160 we obtained indirect blood pressure measurements, at PD 200 the rats were fasted for 18 hours and then an oral glucose‐tolerance test was administered. At this point, the rats were then placed in an operant paradigm to examine for differences in motivation to obtain a palatable food, given the differences in their prenatal and diet histories. These studies are currently under way; preliminary results suggest rats on the high‐fat diets have reduced glucose tolerance and are significantly heavier than their chow‐fed counterparts. Research supported NIH‐DK064712.