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Effects of High Fat Diet and Exercise Intervention Before and During Pregnancy on the Hearts of C57BL/6 Mothers
Author(s) -
Grue Katherine A.,
Kaur Gurvinder,
Joiner Hayli E.,
Jacobo A. Unique,
Ramalingam Latha,
Shen ChwanLi,
Dufour Jannette M.,
MoustaidMoussa Naima,
Chung Eunhee
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.1239.8
Subject(s) - medicine , endocrinology , insulin resistance , pregnancy , gestation , fetus , muscle hypertrophy , mitochondrial biogenesis , biology , insulin , mitochondrion , genetics , microbiology and biotechnology
Obesity is associated with pathological cardiac hypertrophy, while pregnancy and exercise induce physiological cardiac hypertrophy. Unlike physiological growth, pathological cardiac hypertrophy is associated with a re‐expression of fetal genes that are commonly expressed in fetal heart and alteration of cardiac metabolism. Currently, the interactive effects of these stimuli on cardiac adaptation are not well understood. Thus, this study aims to test the hypothesis that exercise before and during pregnancy would alleviate high fat diet induced cardiac maladaptation. Using C57BL/6 virgin female mice as a model, we fed the animals either a high fat diet (45% kcal fat) or a low fat diet (LFD: 10% kcal fat) for twelve weeks. Four weeks prior to pregnancy initiation, the HFD group mice were split into either sedentary (HFD) or exercised mice which participated in voluntary wheel running throughout gestation (HFD+Ex). The study was terminated at gestation day 19. Exercise during pregnancy did not improve HFD induced insulin resistance at day 15 of gestation. However, serum insulin levels at gestation day 19 were significantly reduced in HFD+Ex compared to the HFD suggesting better insulin sensitivity. Re‐expression of fetal genes were not observed in any group. However, hearts from HFD+Ex exhibited significant upregulation of genes regulating lipid and glucose metabolism ( medium‐chain acyl‐coA dehydrogenase, carnitine palmitoyltransferase I, insulin receptor substrate 1, and hexokinase 1 ), and mitochondrial biogenesis ( Peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha ) compared to HFD, but not the LFD. These data suggest that while exercise before and during pregnancy did not alter high fat diet associated whole body insulin resistance, it upregulated the metabolic genes of the heart of pregnant mothers. Our results suggest that exercise may be beneficial for cardiac metabolic health by circumventing high‐fat diet induced fatty acid accumulation in the heart.