Obesity and gestational diabetes T. Sathyapalan a , D. Mellor b , S.L. Atkin a, * a Department of Diabetes, Endocrinology and Metabolism, Hull York Medical School, Hull, UK b Department of Diabetes, Endocrinology and Metabolism, University of Hull, Hull, UK keywords: Gestational diabetes Obesity Oral glucose tolerance test Pregnancy summary The prevalence of both obesity and gestational diabetes mellitus (GDM) is increasing worldwide. GDM affects about 7% of all pregnancies and is defined as any degree of impaired glucose tolerance during gestation. The presence of obesity has a significant impact on both maternal and fetal complications associated with GDM. These complications can be addressed, at least in part, by good glycaemic control during pregnancy. The significance and impact of obesity in women with GDM are discussed in this article, together with treatment options, the need for long-term risk modification and postpartum follow-up. Ó 2009 Elsevier Ltd. All rights reserved. 1. Introduction Pregnancy is associated with physiological insulin resistance and hyperinsulinaemia, features that predispose susceptible women to develop diabetes during pregnancy. This resistance stems from placental secretion of diabetogenic hormones, including growth hormone, cortisol, placental lactogen, and progesterone, as well as increased maternal adipose deposition, reduced exercise, and increased caloric intake. These physiological metabolic changes ensure that the fetus has an ample supply of ‘fuel’ and nutrients. Gestational diabetes mellitus (GDM) occurs when maternal pancreatic islet function is insufficient to match the insulin resistance associated with pregnancy. GDM is defined as any degree of impaired glucose tolerance recognised during pregnancy. Most women with GDM have impaired glucose tolerance manifest only in pregnancy, but some may have type 2 diabetes that was unrecognised prior to pregnancy. The insulin resistance, which is particularly prominent in the second half of pregnancy, is increased by any co-existent conditions associated with increased insulin resistance, so contributing to the development of GDM. In particular, obesity increases insulin resistance 1,2 by a mechanism that may involve higher plasma levels of triglycerides and non-esterified fatty acids, and lower plasma levels of adiponectin. 2. Obesity and GDM The incidence of GDM in pregnancy in women who are obese is higher than that of the general obstetric population (6–12% versus 2–4%). 3,4 GDM occurs in about 8.8% of pregnancies in the developed world and the risk of GDM is directly proportional to maternal body mass index (BMI; kg/m 2 ). The overall risk of developing GDM for women is reported to be 2.9-fold with BMI 30 compared with BMI 20, 5 but estimates vary with the population and BMI cut-off employed, with levels of risk as high as 20-fold reported. 6 In addition to the increased risk of obese women developing GDM, there is also an increased risk of type 2 diabetes, characterised by whole-body insulin resistance and higher plasma insulin concen- trations. Weight loss and healthy lifestyle can help to prevent type 2 diabetes and also appear to reduce the risk of GDM. 7,8 On the other hand, inter-pregnancy weight gain and increasing maternal age worsens the risk of developing GDM. 9,10 The rate of fetal or neonatal death in the offspring of women with type 2 diabetes or GDM is higher than in non-diabetic controls 11 ; this mainly occurs as late fetal death. There is also a strong relationship between the perinatal mortality rate and maternal obesity in pregnant women with type 2 diabetes. Major complications of labour in obese women (pre-gravid BMI 30, compared with controls with pre-gravid BMI 30) include labour induction failure, failure to progress in the first stage of labour, meconium-stained amniotic fluid, malpresentation, and shoulder dystocia. 12 It has been reported that pre-gravid obesity and the severity of GDM predicted an increase in congenital malformations including cleft lip/palate, cardiac, genitourinary, digestive tract and skeletal abnormalities observed in the offspring in 4% of births. 13 The programming of obesity and metabolic syndrome in the * Corresponding author. Address: Michael White Centre for Diabetes, Brockle- hurst Building, Hull Royal Infirmary, Anlaby Road, Hull HU3 2JZ, UK. Tel.: þ44 1482 675365; Fax: þ44 1482 5370. E-mail address: Stephen.atkin@hyms.ac.uk (S.L. Atkin). Contents lists available at ScienceDirect Seminars in Fetal & Neonatal Medicine journal homepage: www.elsevier.com/locate/siny 1744-165X/$ – see front matter Ó 2009 Elsevier Ltd. All rights reserved. doi:10.1016/j.siny.2009.09.002 Seminars in Fetal & Neonatal Medicine 15 (2010) 89–93