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

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. AbstractIn 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.

Elevated maternal linoleic acid reduces circulating leptin concentrations, cholesterol levels and male fetal survival in a rat model

“…; Howell & Powell, ; Musial et al . ; Ye et al . ); however, our study is the first to focus on the effect of consuming high levels of LA with matched total fat and n‐3 content on offspring outcomes, and maternal circulating factors that may affect fertility and development.…”

A high-throughput platform for detailed lipidomic analysis of a range of mouse and human tissues

“…The pipeline we developed was applied to investigate the lipid profile of two groups of mice (one lean and one obese) that represent a model of obesity with gestational diabetes [18][19][20]. Mouse brain, liver, heart, kidney, vastus lateralis muscle, and adipose tissue were run in the same sample batch with serum from the same individual animals.…”

Global mRNA and Long Non-Coding RNA Expression in the Placenta and White Adipose Tissue of Mice Fed a High-Fat Diet During Pregnancy

“…The results indicated that HFD or overnutrition during pregnancy increased the expression of the genes involved in ECM interactions and metabolic pathways, might promote placental development, and ultimately lead to an overgrowth of the foetus. Many studies using an obesogenic diet before or during gestation have demonstrated that a high-sugar diet or HFD increases the expression of glucose and amino acid transporters in the placenta and ultimately induces foetal growth [27] [28][29][30]. However, our results did not reveal any glucose or amino acid transporter proteins to be differentially expressed but indicated increased expression of genes involved in ECM interactions and metabolic pathways, may indicate nutrients from the maternal diet might not directly influence the RNA levels of nutrient transporter genes in the placenta but promote placental development and ultimately lead to foetal growth.…”