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A Western-style obesogenic diet alters maternal metabolic physiology with consequences for fetal nutrient acquisition in mice

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Musial, B 
Vaughan, OR 
Fernandez-Twinn, DS 
Voshol, P 
Ozanne, SE 


In the Western world, obesogenic diets containing high fat and high sugar (HFHS) are commonly consumed during pregnancy. However, the impacts of a HFHS diet during pregnancy on maternal insulin sensitivity and signalling in relation to feto-placental growth and glucose utilization are unknown. The present study examined the effects of a HFHS diet during mouse pregnancy on maternal glucose tolerance and insulin resistance, as well as, on feto-placental glucose metabolism. Female mice were fed a control or HFHS diet from day (D) 1 of pregnancy (term = D20.5). At D16 or D19, dams were assessed for body composition, metabolite and hormone concentrations, tissue abundance of growth and metabolic signalling pathways, glucose tolerance and utilization and insulin sensitivity. HFHS feeding perturbed maternal insulin sensitivity in late pregnancy; hepatic insulin sensitivity was higher, whereas sensitivity of the skeletal muscle and white adipose tissue was lower in HFHS than control dams. These changes were accompanied by increased adiposity and reduced glucose production and glucose tolerance of HFHS dams. The HFHS diet also disturbed the hormone and metabolite milieu and altered expression of growth and metabolic signalling pathways in maternal tissues. Furthermore, HFHS feeding was associated with impaired feto-placental glucose metabolism and growth. A HFHS diet during pregnancy therefore causes maternal metabolic dysfunction with consequences for maternal nutrient allocation for fetal growth. These findings have implications for the health of women and their infants, who consume HFHS diets during pregnancy.



fetal growth, gestational diabetes, glucose metabolism, insulin resistance, nutrient partitioning, pregnancy

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Journal of Physiology

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Medical Research Council (MC_UU_12012/4)
Medical Research Council (MC_UU_12012/5)
Medical Research Council (G0600717)
British Heart Foundation (None)
Medical Research Council (MC_PC_12012)
Medical Research Council (G0600717/1)
We are grateful to the Medical Research Council (MRC) for funding the research through a studentship to BM (MR/J500458/1), an in vivo skills award (MRC CORD G0600717) and the MRC Metabolic Diseases Unit (MC_UU_12012/4).