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
. 2010 Sep;140(3):365-71.
doi: 10.1530/REP-10-0088. Epub 2010 May 10.

Obesity, insulin resistance, and pregnancy outcome

Patrick M Catalano  1
Affiliations
Review

Obesity, insulin resistance, and pregnancy outcome

Patrick M Catalano. Reproduction. 2010 Sep.

Abstract

There has been a significant increase over the past few decades in the number of reproductive age women who are either overweight or obese. Overweight and obese women are at increased risk for having decreased insulin sensitivity as compared with lean or average weight women. The combination of obesity and decreased insulin sensitivity increases the long-term risk of these individuals developing the metabolic syndrome and associated problems of diabetes, hypertension, hyperlipidemia, and cardiovascular disorders. Because of the metabolic alterations during normal pregnancy, particularly the 60% decrease in insulin sensitivity, overweight and obese women are at increased risk of metabolic dysregulation in pregnancy, i.e. gestational diabetes, preeclampsia, and fetal overgrowth. Hence, pregnancy can be considered as a metabolic stress test for the future risk of the metabolic syndrome. In this review, we will review the underlying pathophysiology related to these disorders. Most importantly, an understanding of these risks provides an opportunity for prevention. For example, a planned pregnancy offers an opportunity to address weight control prior to conception. At the very least, by avoiding excessive weight gain during pregnancy, this may prevent excessive weight retention post partum. Finally, based on the concept of in utero programming, these lifestyle measures may not only have short- and long-term benefits for the woman but also for her offspring as well.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Proposed mechanism by which TNF-alpha may decrease insulin sensitivity. TNF-alpha activates a pathway that increases sphingomyelinases and ceramides and may interfere with insulin receptor 1 (IRS-1) autophosphorylation.
Figure 2
Figure 2
Insulin sensitivity in intravenous glucose tolerance assessed by minimal model analysis in women with preeclampsia and normotensive control women (A) during pregnancy and (B) 12 weeks after delivery. Data are mean ± SE (Kaaja et al. 1999)
Figure 3
Figure 3
The longitudinal changes in insulin sensitivity in normal glucose tolerant women as estimated by the hypoinsulinemic-euglycemic clamp. Early pregnancy, 12–14 weeks and late pregnancy 34–36 weeks, longitudinal changes over time, p=0.0001. (Adapted from Catalano et al. 1991)
Figure 4
Figure 4
The longitudinal change in insulin sensitivity in normal glucose tolerant women (CTL) and women with gestational diabetes (GDM). Early pregnancy 12–14 weeks and late pregnancy 34–36 weeks. Changes over time; p=0.0001, changes between groups; p=0.03. (Adapted from Catalano et al. 1999)
Figure 5
Figure 5
The longitudinal changes in insulin sensitivity in average (BMI<25), overweight (BMI 25–30) and obese (BMI>30) women over time. Early pregnancy 12–14 weeks and late pregnancy 34–36 weeks longitudinal changes over time; p=0.0004. (Adapted from Catalano & Ehrenberg 2006)
Figure 6
Figure 6
Body composition in neonate of women with normal glucose tolerance (CTL) and gestational diabetes (GDM)

  1. Lean body mass (LBM); p=0.74

  2. Fat mass (FM); p=0.0002

  3. Percent body fat (%BF); p=0.0001

(Adapted from Catalano et al. 2003)
Figure 7
Figure 7
Body composition in neonates of lean/average (Body mass index [BMI] <25kg/m2) and overweight/obese (BMI >25 kg/m2) women

  1. Lean body mass (LBM); p=0.22

  2. Fat mass (FM); p=0.0008

  3. Percent body fat (%BF); p=0.006

(Adapted from Sewell et al. 2006)
Figure 8
Figure 8
Proposed model of fetal programming of offspring of women with abnormal metabolic environment (increased insulin resistance) (Adapted from Catalano 2003)
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Ananth CV, Wen SW. Trends in fetal growth among singleton gestations in the United States and Canada. Seminars in Perinatology. 2002;26:260–267. - PubMed
    1. Ausman LM, Powell EM, Mercado DL, Samonds KW, el Lozy M, Gallina DL. Growth and developmental body composition of the cebus monkey (Cebus Albifrons) American Journal Perinatology. 1982;3:211–217. - PubMed
    1. Barton JR, Sibai BM. Prediction and prevention of recurrent preeclampsia. Obstetrics and Gynecology. 2008;112:359–372. - PubMed
    1. Bergman RN, Prager R, Volund A, Ofefsky JM. Equivalence of the insulin sensitivity index in man derived by the minimal model method and the euglycemic glucose clamp. Journal of Clinical Investigation. 1987;79:790–800. - PMC - PubMed
    1. Buchanan T, Xiang AH. Gestational diabetes mellitus. Journal of Clinical Investigations. 2005;115:485–491. - PMC - PubMed

Publication types