Maternal fat, but not lean, mass is increased among overweight/obese women with excess gestational weight gain

Berggren, Erica K.; Groh-Wargo, Sharon; Presley, Larraine; Mouzon, Sylvie Hauguel-de; Catalano, Patrick M.

doi:10.1016/j.ajog.2015.12.026

Cited by 57 publications

(45 citation statements)

References 20 publications

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“…Further, our group has already demonstrated that, among overweight/obese women, excess gestational weight gain is comprised of primarily fat, and not fat free, mass. 20 …”

Section: Commentmentioning

confidence: 99%

Variations in resting energy expenditure: impact on gestational weight gain

Berggren

O’Tierney-Ginn

Lewis

et al. 2017

American Journal of Obstetrics and Gynecology

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Background There are significant variations in gestational weight gain with many women gaining in excess of Institute of Medicine guidelines. Unfortunately, efforts to improve appropriate gestational weight gain have had only limited success. To date, interventions have focused primarily on decreasing energy intake and/or increasing physical activity. Maternal resting energy expenditure, which comprises ~60% of total energy expenditure compared with the ~20% that comes from physical activity, may be an important consideration in understanding variations in gestational weight gain. Objective Our objective was to quantify the changes in resting energy expenditure during pregnancy and their relationship to gestational weight gain and body composition changes among healthy women. We hypothesized that greater gestational weight gain, and fat mass accrual in particular, are inversely related to variations in resting energy expenditure. Study design We conducted a secondary analysis of a prospective cohort studied preconception and late (34–36 weeks) pregnancy. Body composition (estimated using air densitometry, BodPod) and resting energy expenditure (estimated using indirect calorimetry) were measured. The relationship between changes in resting energy expenditure and gestational weight gain, and change in fat mass and fat free mass were quantified. Resting energy expenditure was expressed as kilocalories per kilogram of fat free mass per day (kcal.kg FFM−.day−1) and kilocalories per day (kcal/day). Correlations are reported as r. Results Among 51 women, preconception body mass index was 23.0 (4.7) kg/m2; gestational weight gain was 12.8 (4.7) kg. Preconception and late pregnancy resting energy expenditure (kcal/day) correlated positively with the change in fat free mass (r=0.37, p=0.008; r=0.51, p=0.001). Late pregnancy resting energy expenditure (kcal.kg FFM−.day−1) was inversely associated with the change in fat mass (r=−0.34, p=0.02) and gestational weight gain (r=−0.29, p=0.04). From pre-pregnancy through late gestation, the increase in resting energy expenditure (kcal/day) correlated positively with the change in fat free mass (r=0.44, p=0.002), and negatively with the change in fat mass (r=−0.27, p=0.06). Conclusions The change in resting energy expenditure from preconception through late gestation correlated positively with changes in fat free mass but negatively with fat mass accrual. Women with smaller increases in resting energy expenditure across pregnancy had greater gestational weight gain, specifically more adipose tissue. These data suggest that resting energy expenditure is an important factor in gestational weight gain, particularly excess fat mass accrual. Future lifestyle intervention studies need to consider clinically feasible means of estimating resting energy expenditure and, in response, tailor nutrient intake and composition recommendations. Implementing and testing such interventions would be a novel approach to improve compliance with gestational weight gain guidelines.

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“…Further, our group has already demonstrated that, among overweight/obese women, excess gestational weight gain is comprised of primarily fat, and not fat free, mass. 20 …”

Section: Commentmentioning

confidence: 99%

Variations in resting energy expenditure: impact on gestational weight gain

Berggren

O’Tierney-Ginn

Lewis

et al. 2017

American Journal of Obstetrics and Gynecology

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“…; Berggren et al . ). 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, ; Berggren et al .…”

Section: Introductionmentioning

confidence: 97%

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

Musiał

Vaughan

Fernandez‐Twinn

et al. 2017

The Journal of Physiology

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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.

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“…Of particular concern is the increased risk to the offspring for excess neonatal adiposity and metabolic disease in adolescence and adulthood [3, 4]. Other obesity-related traits, including insulin resistance, are associated with fetal macrosomia [5–8]. However, the causal nature of the factors that result in higher fetal body adiposity remain to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

Causal relationship between obesity-related traits and TLR4-driven responses at the maternal–fetal interface

Yang

Haghiac

et al. 2016

Diabetologia

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Aims/hypothesis Obesity triggers complex inflammatory networks within the innate immune system. During pregnancy, the placenta amplifies the low-grade inflammation through activation of Toll-like receptor 4 (TLR4) signalling pathways. The purpose of this study was to investigate the impact of obesity on placental TLR4 expression and inflammatory signals. The secondary aim was to analyse the placental cell type responsible for TLR4 activation. Methods Thirty-nine women recruited at term-scheduled Caesarean section were grouped according to their pre-gravid BMI (< 25 kg/m2 and > 30 kg/m2). Placenta, venous maternal and cord blood were obtained at delivery for analysis. Data were analysed with linear regression and Spearman’s rank correlation coefficient analysis. Results TLR4, IL6 and IL8 expression was increased three- to ninefold (p < 0.001) in the placenta of obese vs lean women. There was a positive correlation between placental TLR4 and maternal systemic and placental IL6 and IL8 concentrations. Placental TLR4 expression was correlated with maternal pre-gravid BMI, insulin resistance index, plasma insulin and C-reactive protein (r = 0.57, 0.31, 0.35, 0.53, respectively; p < 0.001) but not with plasma glucose, maternal age, gestational age and gestational weight gain (r < 0.2; p > 0.1). TLR4 was located in both trophoblast and macrovascular endothelial cells lining fetal vasculature. Lipopolysaccharide-induced TLR4 activation was more robust in trophoblasts than in endothelial vascular cells (100-fold vs tenfold; p < 0.001). Conclusions/interpretation Trophoblastic TLR4 is implicated in the propagation of placental inflammation. Placental inflammation is related to maternal metabolic conditions such as pre-gravid BMI, whilst gestational weight gain or gestational age are not. These results implicate the pre-gravid condition as a significant contributor to metabolic inflammation in late pregnancy.

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Maternal fat, but not lean, mass is increased among overweight/obese women with excess gestational weight gain

Cited by 57 publications

References 20 publications

Variations in resting energy expenditure: impact on gestational weight gain

Variations in resting energy expenditure: impact on gestational weight gain

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

Causal relationship between obesity-related traits and TLR4-driven responses at the maternal–fetal interface

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