Abstract
Intrauterine growth restriction (IUGR) is associated with an increased risk of developing obesity, insulin resistance and cardiovascular disease. However, its effect on energetics in heart remains unknown. In the present study, we examined respiration in cardiac muscle and liver from adult mice that were undernourished in utero. We report that in utero undernutrition is associated with impaired cardiac muscle energetics, including decreased fatty acid oxidative capacity, decreased maximum oxidative phosphorylation rate and decreased proton leak respiration. No differences in oxidative characteristics were detected in liver. We also measured plasma acylcarnitine levels and found that short-chain acylcarnitines are increased with in utero undernutrition. Results reveal the negative impact of suboptimal maternal nutrition on adult offspring cardiac energy metabolism, which may have life-long implications for cardiovascular function and disease risk.
Highlights
The developmental programming hypothesis proposes that adverse influences during critical periods in development permanently alter tissue structure and function, which may have persistent consequences for the long-term health of the offspring [1]
Data are shown for adenylate free leak respiration (LN; A), maximal electron flow through electron-transferring flavoprotein and fatty acid oxidative capacity (PETF; B), maximum oxidative phosphorylation capacity (POXPHOS; C) and oligomycin-induced leak respiration (Lomy; D)
We show that in utero undernutrition in mice results in impaired cardiac muscle energetics without altering mitochondrial content and that this is associated with increased
Summary
The developmental programming hypothesis proposes that adverse influences during critical periods in development permanently alter tissue structure and function, which may have persistent consequences for the long-term health of the offspring [1]. Epidemiological studies in humans and animal models have shown that intrauterine growth restriction (IUGR) is associated with an increased risk of developing obesity, insulin resistance and cardiovascular disease in the offspring [2]. Previous research in mice has shown that 50 % food restriction during late pregnancy leads to IUGR, low birth weight and offspring that develop progressive, severe glucose intolerance and β-cell dysfunction [8,9]. Using this model, we previously showed that these low birth weight offspring have increased adiposity, decreased skeletal muscle energetics in mixed muscle and a blunted weight loss response to a hypocaloric diet in adulthood [9].
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