Sendai [Japan], April 15 (ANI): According to a new study led by Tohuku University, exercise during pregnancy may also help in reducing the offspring’s chances of getting type 2 diabetes.
The study was published in the journal, ‘Diabetes’. It has also demonstrated that maternal exercise during pregnancy improves the metabolic health of offspring, even when the mother is obese or on a high-fat diet.
Physical exercise by the mother induces the placenta to secrete the key protein SOD3, resulting in a lowered risk of diabetes for the offspring.
Maternal obesity and type 2 diabetes are on the rise. Over 30 per cent of women of childbearing age in Western and Asian countries are classified as obese. Meanwhile, 630 million people are expected to be living with type 2 diabetes by 2045. Children born to obese mothers or mothers with type 2 diabetes have an increased risk of diabetes, even after going on to live healthy lives.
“With the growth of maternal obesity, a worrying cycle is forming where the risks of diabetes get passed down from generation to generation,” said assistant professor Joji Kusuyama from Tohoku University’s Interdisciplinary Institute for Frontier Sciences (FRIS), and lead author of the study.
“Stopping this cycle is a critical and pressing medical problem,” he added.
Previously, researchers showed that exercise during pregnancy has tremendous benefits on an offspring’s metabolic health, demonstrating that placenta-derived SOD3, which stands for superoxide dismutase 3, plays a key role in transmitting the benefits of maternal exercise to the offspring.
Building on this, the team set out to understand how SOD3 prevents the negative effects of obesity from being passed from mother to child and found that SOD3 inhibited high-fat diet-induced abnormalities in the offspring’s glucose metabolism.
Histone methylation plays a fundamental role in epigenetic modification — heritable changes to strands of DNA that do not affect the inherited base pairs. The methyl group (-CH3) attaches to an amino acid in the tail of histone proteins that wraps DNA, sometimes activating gene expression, sometimes inhibiting it.
When a mother consumes a diet heavy in fat, the histone H3 trimethylation H3K4me3 gets decreased in the fetal liver and hinders the expression of glucose metabolism genes.
This, the researchers discovered, is caused by two things. Reactive oxygen species (ROS) — oxygen in a reactivated and activated state that aids the body’s metabolism and cellular functions — becomes elevated. Meanwhile, WDR82, a key protein that regulates histone methyltransferase, becomes oxidative, impairing protein functions.
The harmful effects of a maternal high-fat diet on an offspring’s metabolism are reversed by maternal exercise.
Genetic manipulation demonstrated that placental SOD3 is indispensable for the protective effects of maternal exercise on offspring.
The study also highlighted how crucial exercise is for negating this. When the researchers infused N-acetylcysteine (NAC), an antioxidant that boosts performance in the liver, into the fetal liver, it did not reproduce the results of SOD3. This suggested the naturally produced SOD3 from exercise during pregnancy is pivotal for the offspring’s metabolic wellbeing.
Given the simplicity and cost-effectiveness of exercise, encouraging mothers to exercise could help reverse the alarming rates of obesity and type-2 diabetes. The merits of SOD3 may not be limited to the metabolism stresses Kusuyama.
“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,” Kusuyama added.