Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2014 Mar;31(3):292-301.
doi: 10.1111/dme.12382.

Maternal outcomes and follow-up after gestational diabetes mellitus

Affiliations
Review

Maternal outcomes and follow-up after gestational diabetes mellitus

C Kim. Diabet Med. 2014 Mar.

Abstract

Gestational diabetes mellitus reflects impaired maternal insulin secretion relative to demand prior to pregnancy, as well as temporary metabolic stressors imposed by the placenta and fetus. Thus, after delivery, women with gestational diabetes have increased risk of diabetes and recurrent gestational diabetes because of their underlying impairment, which may be further exacerbated by fat accretion during pregnancy and post-partum deterioration in lifestyle behaviours. This hypothetical model is discussed in greater detail, particularly the uncertainty regarding pregnancy as an accelerator of β-cell decline and the role of gestational weight gain. This report also presents risk estimates for future glucose intolerance and diabetes and reviews modifiable risk factors, particularly body mass and lifestyle alterations, including weight loss and breastfeeding. Non-modifiable risk factors such as race/ethnicity and insulin use during pregnancy are also discussed. The review concludes with current literature on lifestyle modification, recommendations for post-partum glucose screening, and future directions for research to prevent maternal disease.

PubMed Disclaimer

Conflict of interest statement

Competing interests

None declared.

Figures

Figure 1
Figure 1
Pre-conception maternal insulin sensitivity and secretion, in conjunction with placental and fetal hormone production, influence intra-partum maternal fat accumulation as well as insulin secretion and sensitivity. Thus, post-partum glucose tolerance reflects pre-conception metabolism altered by the adipose tissue gained during pregnancy, possibly stresses upon the pancreatic β-cell possibly accelerated by the pregnancy, fat stores accumulated during pregnancy and retained after delivery and post-partum behaviours.

References

    1. Metzger B, Buchanan T, Coustan D, De Leiva A, Dunger D, Hadden D, et al. Summary and recommendations of the Fifth International Workshop—Conference on Gestational Diabetes Mellitus. Diabetes Care. 2007;30:S251–S260. - PubMed
    1. IADSPG Consensus Panel. International Association of Diabetes and Pregnancy Study Groups recommendations on the diagnosis and classification of hyperglycemia in pregnancy. Diabetes Care. 2010;33:676–682. - PMC - PubMed
    1. Xiang A, Kjos S, Takayanagi M, Trigo E, Buchanan T. Detailed physiological characterization of the development of type 2 diabetes in Hispanic women with prior gestational diabetes mellitus. Diabetes. 2010;59:2625–2630. - PMC - PubMed
    1. Handwerger S, Freemark M. The roles of placental growth hormone and placental lactogen in the regulation of human fetal growth and development. J Pediatr Endocrinol Metab. 2000;13:343–356. - PubMed
    1. McIntyre H, Chang A, Callway L, Cowley D, Dyer A, Radaelli T, et al. Hormonal and metabolic factors associated with variations in insulin sensitivity in normal pregnancy. Diabetes Care. 2010;33:356–360. - PMC - PubMed

Publication types

MeSH terms