Abstract
Key points In the Western world, obesogenic diets containing high fat and high sugar (HFHS) are commonly consumed during pregnancy, although their effects on the metabolism of the mother, in relation to feto‐placental glucose utilization and growth, are unknown.In the present study, the consumption of an obesogenic HFHS diet compromised maternal glucose tolerance and insulin sensitivity in late pregnancy in association with dysregulated lipid and glucose handling by the dam.These maternal metabolic changes induced by HFHS feeding were related to altered 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 obesogenic diets during pregnancy. 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.
Highlights
In the developed Western world, women of child-bearing age obtain a high proportion of their energy intake from fat and/or sugar (Balanza et al 2007; Temme et al 2010; Austin et al 2011)
high fat and high sugar (HFHS) diet reduced both fetal and placental weight on D16, whereas only placental weight remained significantly decreased on D19 (Tables 1 and 2)
The present study shows that excessive consumption of fat and sugar, typical of a Western-style diet compromises maternal glucose tolerance and insulin sensitivity during late mouse pregnancy
Summary
In the developed Western world, women of child-bearing age obtain a high proportion of their energy intake from fat and/or sugar (Balanza et al 2007; Temme et al 2010; Austin et al 2011). Mothers gaining excess weight during pregnancy have a greater probablility of retaining the weight post-delivery and are at increased risk of obesity, type-2 diabetes and cardiovascular disease later in life (Frias & Grove, 2012; Berggren et al 2016) Their infants are often of abnormal birth weight and more prone to obesity, hypertension and type-2 diabetes as adults (Thorsdottir et al 2002; Oken et al 2007; Frias & Grove, 2012). The mechanisms operating during pregnancy that mediate the programming effects of these diets on the mother and her offspring remain largely unknown
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