Abstract
The developmental origins of health and disease hypothesis proposes that an adverse early life environment, including in utero exposure to a maternal obesogenic environment, can lead to an increased long-term risk of obesity and related metabolic complications in offspring. We assessed whether maternal supplementation with conjugated linoleic acid (CLA) could prevent some of these adverse effects in offspring exposed to a maternal high fat diet. Sprague-Dawley dams consumed either a: control (CD), control with CLA (CLA), high fat (HF) or high fat with CLA (HFCLA) diet 10 days prior to mating and throughout pregnancy/lactation. Male offspring were weaned onto a standard chow diet. Body composition was quantified by DXA and oral glucose tolerance tests conducted on adult offspring. Gene/protein expression and histological analysis were conducted in adipose tissue. Offspring from HF dams had increased body weight, body fat deposition, impaired insulin sensitivity and adipocyte hypertrophy; all of which were rescued in HFCLA offspring. Molecular and histological analyses of the adipose tissue suggest that disturbances in adipogenesis may mediate the metabolic dysfunction observed in HF offspring. Therefore, CLA supplementation to a maternal obesogenic diet may be a promising strategy to prevent adverse programming outcomes.
Highlights
The developmental origins of health and disease hypothesis proposes that an adverse early life environment, including in utero exposure to a maternal obesogenic environment, can lead to an increased long-term risk of obesity and related metabolic complications in offspring
While there were no significant differences between weights of offspring from high fat (HF) and high fat with CLA (HFCLA) mothers from P23-122, significant differences were present from P125-140
Dual-energy X-ray absorptiometry (DXA) scans revealed that HF offspring had significantly greater fat mass when expressed relative to body weight (Fig. 2A) and in absolute terms in grams (Fig. 2B) compared to control diet (CD) and HFCLA offspring
Summary
The developmental origins of health and disease hypothesis proposes that an adverse early life environment, including in utero exposure to a maternal obesogenic environment, can lead to an increased long-term risk of obesity and related metabolic complications in offspring. Human mesenchymal stem cells from infants of obese mothers display enhanced adipogenic potential[5] These studies suggest that maternal obesity may program an increased propensity for lipid storage in postnatal life. The c9,t11 isomer has been reported to promote adipogenesis through induction of peroxisome proliferator-activated receptor-γ (PPARγ)[13] This may be considered advantageous as it counteracts adipocyte hypertrophy, which can lead to inflammation and dysregulation of the adipose tissue[14]. CLA supplementation to a HF diet blunted the adverse early life growth trajectory (including reduced fetal size and accelerated growth in the pre-weaning period) in offspring from HF dams[16]. The present study investigated the impact of maternal supplementation with mixed CLA isomers to a control and HF diet on whole-body metabolism, adipocyte morphology and adipose tissue function in adult male offspring
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