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Gestational high‐fat feeding impairs female offspring energy metabolism in mice (LB777)
Author(s) -
Guidotti Stefano,
Qiao Liping,
Sun Yoo Hyung,
Shao Jianhua
Publication year - 2014
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.28.1_supplement.lb777
Subject(s) - offspring , endocrinology , medicine , skeletal muscle , white adipose tissue , biology , adipose tissue , calorie , lean body mass , gestation , obesity , pregnancy , body weight , genetics
Maternal obesity and excessive gestational weight gain increase the risk of offspring to the development of obesity and metabolic defects later in life. The present study aimed to elucidate the effects of gestational high‐fat (HF) feeding on offspring energy metabolism and its underlying mechanisms. Pregnant C57BL/6J mice received HF diet (60% calories from fat) or chow from conception until parturition. After delivery, all dams and offspring were fed with chow. Body composition was monitored by echoMRI throughout the study. At 3 months of age, significantly increased body adiposity and reduced lean body mass (LBM) were observed in female offspring from HF‐fed dams without changes in body weight. Female offspring displayed similar energy intake with reduced energy expenditure (EE). When normalized by LBM, EE was no different between groups. No difference was found in UCP‐1 protein levels in brown adipose tissue and in expression of mitochondrial markers in skeletal muscle. Investigating the molecular mechanism underlying this metabolic phenotype, we found a significant reduction in β‐catenin protein levels in skeletal muscle and white adipose tissue. We also observed a reduction in GSK3‐β phosphorylation and other downstream targets of wnt signaling. Together our data indicate that gestational HF‐feeding increases body adiposity in expense of LBM in female offspring. Suppression of the wnt/ β‐catenin signaling in skeletal muscle could potentially lead to deranged muscle development and hence be related to the reduction in LBM. This defect in muscle development may ultimately lead to reduced energy needs, supporting a mechanism aimed at energy conservation that favors the storage of fat.