In general, children born to obese mothers are at risk for obesity or other health problems. But exactly what happens in the womb that causes obesity to be transmitted from mother to child remains unclear. However, a recent study suggests that the placenta is an important factor behind this phenomenon, and suggests that a class of hormones acting on the placenta can protect offspring mice from the adverse effects of obese mothers. While some researchers remain skeptical of the findings, the results suggest a way to avoid risks for people with genetic obesity. Decades ago, researchers found that the womb increases the fetus’ sensitivity to some health problems. People who became pregnant during the Dutch famine of 1944 suffered from higher levels of cardiovascular disease, diabetes, cancer, etc. later in life.
Recent animal experiments have shown that insufficient nutrient supply in the womb can cause changes in DNA expression profiles that can carry genetic diseases to the next generation. But the researchers are also interested in another effect in the womb, the genetic control of overnutrition. They found that obese pregnant women who gave birth tended to have larger offspring, higher body fat, and a higher risk of metabolic diseases, including obesity, high blood sugar, and more.
In order to find the root cause of fetal obesity, developmental scientists at the University of Colorado set their sights on the placenta, the only way to connect the fetus with the mother, and the only way for the fetus to absorb nutrients in the mother. The placenta has been considered a “passive” organ in the past, no matter what happens to the mother, it is passed on to the fetus in one way or another without exception. However, recent research has found that the placenta acts more like a floodgate, selectively filtering out some things.
The placenta delivers maternal nutrition on the one hand, relying on insulin, a hormone that promotes the absorption of sugar by muscle and fat cells and lowers blood sugar levels. During pregnancy, the sensitivity of the mother’s cells to insulin is greatly reduced, so that substances such as sugar, fat, and essential amino acids in the blood are supplied and passed through the placenta. At the same time, insulin can also maintain the activity of transporters, thereby improving the efficiency of nutrients entering the fetus. Because obese/diabetic pregnant women have higher insulin levels and insulin resistance than normal, this system can be overutilized, resulting in fetal obesity.
So the researchers wanted to use other hormones to “fight fire with fire.” They chose a class of hormones called adiponectin, a molecule produced by fat cells that regulates insulin activity in two different ways. First, adiponectin can improve the resistance of muscle cells to insulin and lower blood sugar; second, it can inhibit the activity of insulin in the placenta and hinder the transport of nutrients. Under normal circumstances, the content of adiponectin in obese patients is low, so the authors hope to control this unfavorable phenomenon by artificially increasing the level of this hormone.
