Maternal obesity increases diabetes risk for female offspring

Maternal obesity increases diabetes risk for female offspring

Maternal obesity has been associated with diabetic complications in the resulting offspring, according to experiments in mice reported recently by researchers at the University of Louisville.

Obesity is presently a worldwide health issue, and it is commonly considered a risk factor for diabetes, cardiovascular disease, and stroke. When a pregnant woman is obese, her children can be affected by malformation, functional abnormalities, obesity, and type II diabetes. Since, presently, over 18% of American women are classified as obese, and between 18 and 38% of pregnant women meet this criteria, it is an important issue in maternal and child health in this country. However, very little is known about the mechanism of the link between maternal obesity and diabetic effects in offspring.

To investigate this association, Dr. Jianxiang Xu and Junying Han of the University of Louisville first established a viable animal model to function similarly to maternal diabetes might in humans. Female mice, genetically predisposed to obesity and further marked with a yellow coat color, were mated with normal mice, whose offspring could then be classified by coat color for this obesity gene. The obesity prone mice were obese between 6 and 8 weeks of age, but maintained normal blood glucose levels. Offspring from these and from normal crosses were then fed with normal food for up to 15 weeks, then fed with a high fat diet, and examined by sex, and the mother's obesity status. In this first portion of the study, the birth weight of offspring from obese mothers was 14% higher than in the control group.

When the offspring, at 50 weeks of age, were administered 2 mg glucose per kg body weight. This resulted in similar glucose levels in each group, but major differences in the serum insulin levels. Namely, in female offspring from obese mothers, there was a significant increase in serum insulin levels, while females from obese mothers and males showed no significant differences. This indicates that β cell function was impaired in the female offspring of obese mothers.

To confirm this link, a second experiment was performed. Pancreatic cells were isolated from 50 week old offspring to be tested in vitro for insulin excretion. Cells from mice with a normal diet showed normal secretion, but in the high fat diet, insulin secretion was sharply reduced in offspring from an obese mother, especially when exposed to a high glucose concentration. The measure of other enzymes related to glucose metabolism such as transketolase, GAPDH, and PFK in the cells of the 50 week old mice indicated a decrease in production by the β cells ranging from 31% to 70% for those born to an obese mother.

According to the researchers, this shows that obesity in pregnancy is a factor by itself to impaired glucose tolerance in offspring, which could contribute to the development of gestational diabetes in the mother and type II diabetes in the offspring. Additionally, since there are many mothers who are obese without displaying gestational diabetes, this obesity might be a greater factor in the health of their children than previously expected.

Researchers reported in the journal Endocrinology (May 2013 issue) that obesity susceptibility may be inherited from the grandmother

Jennifer Cropley: Maternal obesity and diabetes: programming heritable disease risk (Video Medical And Professional 2020).

Section Issues On Medicine: Disease