Stress during pregnancy leads to abdominal obesity in mice offspring

ScienceDaily (July 31, 2012) — New research suggests that the neuropeptide Y in plasma and its Y2 receptor in visceral fat play an important role in obesity.

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A new report involving mice suggests that a relationship exists between maternal metabolic or psychological stress and the development of obesity, type 2 diabetes, and metabolic syndrome in her offspring. What's more, the report shows that if the stress cannot be reduced or eliminated, manipulating the neuropeptide Y (NPY) system in visceral fat may prevent maternal stress-induced obesity from occurring in the next generation. This discovery is reported in the August 2012 issue of The FASEB Journal.

"Obesity is a worldwide disease. Here we found that maternal stress, psychologically and metabolically, increases abdominal obesity and glucose intolerance in the next generation in a sex-specific manner, which is mediated by the NPY system in visceral fat," said Ruijun Han, a researcher involved in the work from the Department of Integrative Biology and Physiology, Stress Physiology Center at the University of Minnesota. "Our study suggested that NPY in the platelet-rich plasma and its Y2 receptor in the visceral fat, play an important role in maternal stress-programmed abdominal obesity and metabolic syndrome in offspring."

To make this discovery, Young and colleagues fed different groups of pregnant mice a low protein diet during pregnancy and lactation; a normal protein diet during pregnancy and lactation; or a low protein diet only during pregnancy. After weaning, all the pups were fed high fat diets for 18 weeks, and metabolic parameters and expression of NPY system in periphery tissues were monitored and measured.

"There are a lot of reasons why expectant mothers should not be under stress," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal, "and this report adds yet another reason. What's most interesting, however, is that it provides some insight into how we can counter the negative effects of stress, even when it's not possible to reduce or eliminate the stressors themselves."

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How a low-protein diet predisposes offspring to adulthood hypertension

ScienceDaily (July 25, 2012) — Studies have shown that the offspring of mothers on a low-protein diet are more likely to develop hypertension as adults. Now, Drs. Gao, Yallampalli, and Yallampalli of the University of Texas Medical Branch at Galveston report that in rats, the high maternal testosterone levels associated with a low-protein diet are caused by reduced activity of an enzyme that inactivates testosterone, allowing more testosterone to reach the fetus and increase the offspring's susceptibility to adulthood hypertension.

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Fetal programming is a term used to describe the impact of maternal stress on an unborn child's physical characteristics at birth, as well as its long-term health. The placenta is thought to be a major contributor to fetal programming due to its critical roles in hormone production and nutrient transport, as well as its susceptibility to environmental disruptions.

Recently, a study found that protein restriction doubles the plasma testosterone levels in pregnant rats. Elevated testosterone levels are associated with pregnancy-related complications such as preeclampsia and polycystic ovarian syndrome in humans, and emerging evidence suggests that testosterone may play a role in fetal programming of hypertension.

Gao et al. hypothesized that the increased testosterone levels were caused either by increased activity of an enzyme that produces testosterone or by decreased activity of an enzyme that reduces testosterone, specifically Hsd17b2, which converts testosterone to a less potent androgen, androstenedione.

The team found that Hsd17b2 expression in rats was affected by protein restriction in two parts of the placenta. It was increased in the junctional zone, which is responsible for hormone production, but was reduced in the labyrinth zone, which is essential for nutrient transport from mother to fetus and also acts as a protective barrier.

Based on this novel finding, Gao et al. propose that the reduction in Hsd17b2 expression in the protective labyrinth zone may allow more testosterone to reach the fetus and play a role in fetal programming of hypertension.

The finding that Hsd17b2 was the only enzyme for testosterone production affected by gestational protein restriction suggests an important role for Hsd17b2 in regulating the testosterone levels at the maternal-fetal interface; further research is needed to determine its exact functions.

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Breathing Smog While Pregnant May Worsen Asthma in Offspring

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Excess weight in pregnant women can have negative health Implications for offspring in adulthood

ScienceDaily (May 13, 2012) — That overweight during pregnancy can lead to overweight children and adolescents has been known for some time, but new research at the Hebrew University of Jerusalem and in the US indicates that excess weight before and during pregnancy can have long-lasting health consequences for the offspring of such mothers even later in life.

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Investigators at the Hebrew University-Hadassah Braun School of Public Health and Community Medicine and the Departments of Medicine and Epidemiology at the University of Washington, Seattle, have found a direct correlation between this maternal overweight and higher tendencies in their adult children towards overweight and other life-risking factors, such as high blood pressure and excess sugar and fat levels in the blood.

The research -- the results of which were published recently in the journal Circulation -- was based on analysis of clinical information on 1400 people who were born in Jerusalem between the years of 1974-76. The data provided information, among other things on their birth records, including the weights of their mothers before and during pregnancy and the weight of the child at birth. The researchers further gathered current clinical data on the examined group, all at the age of 32, including their weight, blood pressure and sugar and fat levels in the blood, plus measurements of body mass index (BMI) -- a measure of body fat based on height and weight -- as well as hip width.

.The results of the research showed a clear influence of the overweight of the mothers on the overweight of their children, affecting in turn other risk factors in adulthood. Therefore, it may be concluded that avoiding overweight in adulthood could potentially reduce those other risk factors associated with pre-pregnancy and pregnancy overweight.

Thus, for example, the children of mothers who gained more than 14 kilograms (31 pounds) during pregnancy were measured to have a higher BMI than those who were born to mothers who did not gain more than nine kilos (20 pounds) during pregnancy. In terms of hip measurements, the adult children of overweight pregnant mothers had hip widths nearly ten centimeters more, on average, than those who were born to mothers who were not overweight.

Similar comparisons were made regarding sugar and fat levels in the blood, all indicating that those born to overweight mothers had detrimental characteristics regarding their health and life expectancies as compared to those born to mothers who had not gained excessive weight.

Additional factors could also have an influence on the phenomenon, including analogous genetic traits of the mother and child or environmental influences during pregnancy, and these would be worthy of further investigation, say the researchers.

"We know now that events occurring early in life to fetuses have long-lasting consequences for the health of the adult person," said Dr. Hagit Hochner, the leading researcher on the project.

Added Prof. Orly Manor, who also was involved in the project: "In an age of an 'overweight epidemic' in the world, it is important to know the factors that are involved in leading to overweight and other health risks. This understanding makes it essential that we identify those early windows of opportunity in which we can intervene in order to reduce the risks of chronic illness later in life."

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