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Mom's diabetes affects development of her eggs

For the first time, researchers have shown that poorly controlled maternal diabetes has an adverse effect on methylation of the maternal imprinting gene Peg3, which contributes to impaired development in her offspring.

Previous studies have revealed that offspring of diabetic mothers display a higher incidence of malformations and fetal death, even when a one-cell embryo is transplanted from a diabetic to a non-diabetic mother.

The work is published in the journal Biology of Reproduction, published by the Society for the Study of Reproduction on March 5, 2013.

Diabetic mothers' oocytes tend to exhibit reduced glucose
metabolism, compromised communication between cumulus
cells and oocytes, mitochondrial malfunction,
and a decreased ovulation rate, all of which can be traced
back to reduced gene expression in the embryos.

Qing-Yuan Sun and Zhao-Jia Ge of the Chinese Academy
of Sciences hypothesized that the reduced gene expression
results from disturbed DNA re-methylation² during
oogenesis and oocyte maturation.

The team bred and examined three different mouse populations: one with spontaneously occurring diabetes, one with diabetes induced by STZ¹ injection, and one without diabetes. On Day 15, after mating, the diabetic mice presented with reduced pregnancies (approx. 74% vs. 100% in non-diabetic mice) and increased embryo death rates (approx. 16% vs. 0%), consistent with previous reports.

Focusing on the methylation patterns of one paternally methylated gene (H19) and two maternally methylated genes (Peg3 and Snrpn), the team found that none of the mice showed impaired methylation until 35 days after STZ injection; however, embryo development and number of offspring were already affected by Day 15.

On Day 35, methylation of Peg3 was significantly decreased, with an unmethylated oocyte rate nearly 22% higher in both types of diabetic mice compared to controls. H19 remained unaffected and effects on Snrpn were not significant.

As for the female offspring of diabetic mothers,
their oocytes did not appear to have any methylation
abnormalities. However, due to the difficulty of producing
mice offspring conceived after Day 15, it will be extremely
difficult to determine whether those
females are similarly unaffected.

¹Streptozotocin (Streptozocin, STZ, Zanosar®) is a naturally occurring chemical that is particularly toxic to the insulin-producing beta cells of the pancreas in mammals. It is used in medicine for treating certain cancers of the Islets of Langerhans and used in medical research to produce an animal model for Type 1 diabetes in large dose as well as Type 2 diabetes with multiple low doses.

²Methylation is a form of alkylation with, to be specific, a methyl group, rather than a larger carbon chain, replacing a hydrogen atom. These terms are commonly used in chemistry, biochemistry, soil science, and the biological sciences.

Biology of Reproduction, published by the Society for the Study of Reproduction, is a top-rated peer-reviewed research journal in the field of reproductive biology.

Ge ZJ, Liang XW, Guo L, Liang QX, Luo SM, Wang YP, Wei YC, Han ZM, Schatten H, Suna QY. Maternal diabetes causes alterations of DNA methylation statuses of some imprinted genes in murine oocytes. Biol Reprod 2013; (in press). Published online ahead of print _ March 2013; DOI 10.1095/biolreprod.112.105981.

Contact person: Qing-Yuan Sun, State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China. E-mail: sunqy@ioz.ac.cn

Original article: http://www.eurekalert.org/pub_releases/2013-03/sfts-mdi031513.php