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Preparation of Frozen Non-Human Primate Fetal Islets for Combined Single Nuclei RNA-Sequencing and ATAC-Sequencing, and Bulk Metabolomics
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The intrauterine metabolic environment modulates the gene expression pattern in fetal rat islets: prevention by
1Laboratoire de Biologie Cellulaire, Université catholique de Louvain, 5, Place Croix du Sud, 1348, Louvain-la-Neuve, Belgium. brigitte.reusens@uclouvain.be
Insights
Maternal low-protein diet alters fetal islet gene expression, impacting beta cell development and predisposing offspring to diabetes. Taurine supplementation during gestation normalized gene expression, preventing these adverse effects.
Area of Science:
- Endocrinology
- Developmental Biology
- Nutritional Science
Background:
- Fetal development is sensitive to maternal nutrition, with implications for adult health.
- Maternal low-protein (LP) diet during gestation reduces fetal beta cell mass and causes lasting metabolic dysfunction.
- Taurine, essential for fetal development, is suboptimal in mothers on an LP diet, but supplementation prevents abnormalities.
Purpose of the Study:
- To investigate gene expression changes in fetal islets exposed to maternal LP diet.
- To determine how maternal taurine supplementation prevents LP diet-induced gene expression alterations.
Main Methods:
- Pregnant rats were fed control, LP, or LP + taurine diets.
- Fetal pancreases were collected at 21.5 days gestation, and islets were cultured.
- Transcriptome analysis was performed on cultured neoformed islets.
Main Results:
- Maternal LP diet altered over 10% of fetal islet genes, notably affecting the tricarboxylic acid cycle, ATP production, cell proliferation, and defense pathways.
- Maternal taurine supplementation normalized the expression of all diet-altered genes.
Conclusions:
- The intrauterine environment, influenced by maternal nutrition, epigenetically programs fetal beta cell development and respiration.
- Maternal LP diet can program a pre-diabetic phenotype, which is preventable with early taurine intervention.
Aims/Hypothesis:
Events during fetal life may in critical time windows programme tissue development leading to organ dysfunction with potentially harmful consequences in adulthood such as diabetes. In rats, the beta cell mass of progeny from dams fed with a low-protein (LP) diet during gestation is decreased at birth and metabolic perturbation lasts through adulthood even though a normal diet is given after birth or after weaning. Maternal and fetal plasma taurine levels are suboptimal. Maternal taurine supplementation prevents these induced abnormalities. In this study, we aimed to reveal changes in gene expression in fetal islets affected by the LP diet and how taurine may prevent these changes.
Methods:
Pregnant Wistar rats were fed an LP diet (8% [wt/wt] protein) supplemented or not with taurine in the drinking water or a control diet (20% [wt/wt] protein). At 21.5 days of gestation, fetal pancreases were removed, digested and cultured for 7 days. Neoformed islets were collected and transcriptome analysis was performed.
Results:
Maternal LP diet significantly changed the expression of more than 10% of the genes. Tricarboxylic acid cycle and ATP production were highly targeted, but so too were cell proliferation and defence. Maternal taurine supplementation normalised the expression of all altered genes.
Conclusions/Interpretation:
Development of the beta cells and particularly their respiration is modulated by the intrauterine environment, which may epigenetically modify expression of the genome and programme the beta cell towards a pre-diabetic phenotype. This mis-programming by maternal LP diet was prevented by early taurine intervention.
