Research emerging from Japan’s Tohoku University suggests that exercising during pregnancy can considerably benefit the mother’s child, reducing their risk of Type 2 diabetes.
The Tohoku University study identified that exercising during pregnancy enhanced the metabolic health of offspring, even when the mother is obese on consuming a high-fat diet. The maternal exercise was discovered to influence the placenta to secrete SOD3, an essential protein that effectively lowers diabetes risk in the offspring.
The findings of the research are published in the journal Diabetes.
Maternal obesity and Type 2 diabetes: A growing problem
Data demonstrates that maternal obesity and Type 2 diabetes cases are increasing annually, with over 30% of childbearing age in Western and Asian countries being classified as obese. In addition, it is estimated that 630 million people will be living with Type 2 diabetes by 2045 and children born to obese mothers or Type 2 diabetes are at an elevated risk of going on to develop the condition, even if they live healthy lives.
Joji Kusuyama, an assistant professor from Tohoku University’s Interdisciplinary Institute for Frontier Sciences (FRIS), and the lead author of the study, commented: “With the growth of maternal obesity, a worrying cycle is forming where the risks of diabetes get passed down from generation to generation. Stopping this cycle is a critical and pressing medical problem.”
The team’s previous research highlighted that exercising during pregnancy had considerable benefits for the child’s metabolic health, showing that the placenta-derived SOD3 – also known as supuroexide dismutase 3 – is crucial in transmitting these maternal benefits.
The researchers set out to uncover how SOD3 mitigate the adverse effects of obesity being passed from mother to child, finding that the protein inhibited high-fat diet-induced abnormalities in the offspring’s glucose metabolism.
Impacts of exercising during pregnancy
Histone methylation performs an instrumental role in epigenetic modification, which is heritable changes to strands of DNA that do not affect the inherited base pairs. For example, methyl group (-CH3) attaches to an amino acid in the tail of histone proteins that wraps DNA, either activating or inhibiting gene expression. When a mother eats a high-fat diet, the histone H3 trimethylation H3K4me3 is reduced in the foetal liver, blocking the expression of glucose metabolism genes.
The researcher identified that this is influenced by two factors. The first is reactive oxygen species (ROS) – oxygen in a reactivated and activated state that helps the body’s metabolism and cellular functions – is increased. The second is a key protein called WDR82 that regulates histone methyltransferase becomes oxidative, impairing protein functions.
However, the team discovered that the impacts of a high-fat maternal diet are reversed through exercising during pregnancy, with genetic manipulation showing that placental SOD3 is the key driver of the protective effects of maternal exercise on offspring.
To explore this, the team infused N-acetylcysteine (NAC), an antioxidant that enhances liver performance, into the foetal liver, findings that it did not reproduce the results of SOD3. This illuminates that the natural produced SOD3 from exercising during pregnancy is vital for the offspring’s metabolic wellbeing.
Developing future interventions
Due to exercise being easy to perform and cost-effective, it could be implemented as an effective intervention to mitigate the risk of obesity of Type 2 diabetes, and there may be further benefits.
Kusuyama said: “There may be wider benefits of this protein on other organs in the child. We are currently looking into the modifications in placenta tissue brought about by SOD3 that may have positive lifelong impacts on children.”
The researchers explained that their study is only at the preclinical stage, meaning further studies are required, and additional aspects of the signalling pathway need more investigation.
