Abstract
BackgroundMitochondria are of major importance in oocyte and early embryo, playing a key role in maintaining energy homeostasis. Epidemiological findings indicate that maternal undernutrition-induced mitochondrial dysfunction during pregnancy is associated with the development of metabolic disorders in offspring. Here, we investigated the effects of moderately decreased maternal energy intake during pregnancy on skeletal muscle mitochondrial biogenesis in fetal offspring with pig as a model.MethodsPregnant Meishan sows were allocated to a standard-energy (SE) intake group as recommended by the National Research Council (NRC; 2012) and a low-energy (LE) intake group. Fetal umbilical vein serum and longissimus muscle samples were collected for further analysis on day 90 of pregnancy.ResultsSow and fetal weights and the concentrations of serum growth hormone (GH) and glucose were reduced in LE group. Maternal LE diet decreased the messenger RNA (mRNA) expression of genes involved in mitochondrial biogenesis and function such as peroxisome proliferator-activated receptor gamma coactivator 1α (PPARGC1A), nuclear respiratory factor 1 (NRF1), mitochondrial transcription factor A (TFAM), β subunit of mitochondrial H+-ATP synthase (ATB5B), sirtuin 1 (Sirt1), and citrate synthase (CS). The protein expression of PPARGC1A and Sirt1, intracellular NAD+-to-NADH ratio, and CS activity was reduced in LE group, and accordingly, mitochondrial DNA (mtDNA) content was decreased. Moreover, copper/zinc superoxide dismutase (CuZn-SOD) expression at both mRNA and protein levels and SOD and catalase (CAT) activities were reduced in LE group as well.ConclusionsThe observed decrease in muscle mitochondrial biogenesis and antioxidant defense capacity suggests that moderately decreased maternal energy intake during pregnancy impairs mitochondrial function in fetal pigs.
Highlights
Mitochondria are of major importance in oocyte and early embryo, playing a key role in maintaining energy homeostasis
Serum growth hormone (GH) concentration was significantly decreased (P < 0.05) in LE fetuses compared with SE group, whereas maternal diet had no effect on the concentrations of triglyceride and insulin (P > 0.05)
Previous studies in rodents suggest that maternal nutritional stress causes changes to skeletal muscle mitochondrial function and oxidative metabolism that persist into adult offspring, increasing the risk of type 2 diabetes (T2D) [4, 21]
Summary
Mitochondria are of major importance in oocyte and early embryo, playing a key role in maintaining energy homeostasis. We investigated the effects of moderately decreased maternal energy intake during pregnancy on skeletal muscle mitochondrial biogenesis in fetal offspring with pig as a model. Zou et al Genes & Nutrition (2016) 11:19 syndrome, and many studies have demonstrated that prenatal maternal undernutrition programs offspring mitochondrial function in various tissues of different animal models, such as the pancreatic islet [41] and kidney [9] of rat and the skeletal muscle of sheep [17]. Studies in mice have shown that maternal exposure to a low-protein diet during pregnancy and lactation decreases mitochondrial DNA content and citrate synthase activity and leads to mitochondrial gene expression changes in the offspring liver and skeletal muscle [18, 27]. To our knowledge, no studies have addressed the effects of maternal low-energy (LE) diets on fetal offspring skeletal muscle mitochondrial biogenesis and function
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