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Maternal high‐fat diet and obesity impact palatable food intake and dopamine signaling in nonhuman primate offspring
Author(s) -
Rivera Heidi M.,
Kievit Paul,
Kirigiti Melissa A.,
Bauman Leigh Ann,
Baquero Karalee,
Blundell Peter,
Dean Tyler A.,
Valleau Jeanette C.,
Takahashi Diana L.,
Frazee Tim,
Douville Luke,
Majer Jordan,
Smith M. Susan,
Grove Kevin L.,
Sullivan Elinor L.
Publication year - 2015
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.21306
Subject(s) - offspring , endocrinology , dopamine , medicine , obesity , dopaminergic , weaning , overweight , biology , pregnancy , genetics
Objective To utilize a nonhuman primate model to examine the impact of maternal high‐fat diet (HFD) consumption and pre‐pregnancy obesity on offspring intake of palatable food and to examine whether maternal HFD consumption impaired development of the dopamine system, critical for the regulation of hedonic feeding. Methods The impact of exposure to maternal HFD and obesity on offspring consumption of diets of varying composition was assessed after weaning. The influence of maternal HFD consumption on the development of the prefrontal cortex‐dopaminergic system at 13 months of age was also examined. Results During a preference test, offspring exposed to maternal HFD consumption and obesity displayed increased intake of food high in fat and sugar content relative to offspring from lean control mothers. Maternal HFD consumption suppressed offspring dopamine signaling (as assessed by immunohistochemistry) relative to control offspring. Specifically, there was decreased abundance of dopamine fibers and of dopamine receptor 1 and 2 proteins. Conclusions This study reveals that offspring exposed to both maternal HFD consumption and maternal obesity during early development are at increased risk for obesity due to overconsumption of palatable energy‐dense food, a behavior that may be related to reduced central dopamine signaling.