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Maternal supplementation with an excess of different fat sources during pregnancy and lactation differentially affects feeding behavior in offspring: Putative role of the leptin system
Author(s) -
Sánchez Juana,
Priego Teresa,
García Ana Paula,
Llopis Marina,
Palou Mariona,
Picó Catalina,
Palou Andreu
Publication year - 2012
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.201200211
Subject(s) - offspring , lactation , leptin , pregnancy , endocrinology , biology , medicine , obesity , weaning , weight gain , body weight , genetics
Scope This study investigates the lasting effects of maternal supplementation with different fat sources during pregnancy and lactation on feeding behavior and energy homeostasis of their offspring, and its relation to hypothetical effects in the development of main central structures involved in leptin signaling. Methods and results Offspring of dams supplemented with olive oil, butter, or margarine during late pregnancy and lactation were fed with normal fat (NF) diet until 4‐month‐old, and then with NF or high fat (HF) diet until 6‐month‐old. Results showed that 21‐day‐old margarine group pups presented a higher cell number in the arcuate nucleus (ARC) (females) and higher hypothalamic ObRb/SOCS3 mRNA ratio (males). In adulthood, and under HF diet, they displayed a lower body weight (both genders) and body fat (males) than the butter group, a lower preference for fat food (both genders), and lower leptin levels than the olive oil (both genders) and butter (males) groups. Conclusions Maternal supplementation with different fat sources during the perinatal period may affect the development of hypothalamic structures and hence predisposition to obesity. Margarine, compared with other fats, may program the offspring for increased leptin sensitivity and a lower preference for fat food, thus providing relative protection against body weight gain in adulthood, particularly under an obesogenic environment.