Abstract
The major symptoms of preeclampsia are de novo hypertension and proteinuria during pregnancy, and the clinical diagnosis of preeclampsia has classically been based on these symptoms. However, glucose tolerance defects and insulin resistance are prominent features of preeclampsia but have not been considered significant phenotypes, particularly when establishing animal models of preeclampsia. This review seeks to evaluate the pathomechanical significance of glucose tolerance defects and insulin resistance in the biology of preeclampsia.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
References
Shenoy V, Kanasaki K, Kalluri R. Pre-eclampsia: connecting angiogenic and metabolic pathways. Trends Endocrinol Metab. 2010;21:529–36.
Kanasaki K, Kanasaki M. Angiogenic defects in preeclampsia: what is known, and how are such defects relevant to preeclampsia pathogenesis? Hypertens Res Pregnancy. 2014;1:9.
Catalano PM, Tyzbir ED, Roman NM, Amini SB, Sims EA. Longitudinal changes in insulin release and insulin resistance in nonobese pregnant women. Am J Obstet Gynecol. 1991;165:1667–72.
Catalano PM, et al. Longitudinal changes in basal hepatic glucose production and suppression during insulin infusion in normal pregnant women. Am J Obstet Gynecol. 1992;167:913–9.
Catalano PM, et al. Carbohydrate metabolism during pregnancy in control subjects and women with gestational diabetes. Am J Physiol. 1993;264:E60–7.
Rieck S, Kaestner KH. Expansion of beta-cell mass in response to pregnancy. Trends Endocrinol Metab. 2010;21:151–8. https://doi.org/10.1016/j.tem.2009.11.001.
Ryan EA, Enns L. Role of gestational hormones in the induction of insulin resistance. J Clin Endocrinol Metab. 1988;67:341–7. https://doi.org/10.1210/jcem-67-2-341.
Kuhl C. Aetiology of gestational diabetes. Baillieres Clin Obstet Gynaecol. 1991;5:279–92.
Yogev, et al. Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study: preeclampsia. Am J Obstet Gynecol. 2010;202:255.e1–7. https://doi.org/10.1016/j.ajog.2010.01.024.
Hauguel S, Leturque A, Gilbert M, Girard J. Effects of pregnancy and fasting on muscle glucose utilization in the rabbit. Am J Obstet Gynecol. 1988;158:1215–8.
Hauguel S, Gilbert M, Girard J. Pregnancy-induced insulin resistance in liver and skeletal muscles of the conscious rabbit. Am J Physiol. 1987;252:E165–9.
Leturque A, et al. Glucose utilization rates and insulin sensitivity in vivo in tissues of virgin and pregnant rats. Diabetes. 1986;35:172–7.
Hotamisligil GS, Murray DL, Choy LN, Spiegelman BM. Tumor necrosis factor alpha inhibits signaling from the insulin receptor. Proc Natl Acad Sci U S A. 1994;91:4854–8.
Xiang AH, et al. Multiple metabolic defects during late pregnancy in women at high risk for type 2 diabetes. Diabetes. 1999;48:848–54.
Kirwan JP, et al. TNF-alpha is a predictor of insulin resistance in human pregnancy. Diabetes. 2002;51:2207–13.
Hotamisligil GS, et al. IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance. Science. 1996;271:665–8.
Saghizadeh M, Ong JM, Garvey WT, Henry RR, Kern PA. The expression of TNF alpha by human muscle. Relationship to insulin resistance. J Clin Invest. 1996;97:1111–6. https://doi.org/10.1172/JCI118504.
Sermer M, et al. Impact of increasing carbohydrate intolerance on maternal-fetal outcomes in 3637 women without gestational diabetes. The Toronto Tri-Hospital Gestational Diabetes Project. Am J Obstet Gynecol. 1995;173:146–56.
Sowers JR, Saleh AA, Sokol RJ. Hyperinsulinemia and insulin resistance are associated with preeclampsia in African-Americans. Am J Hypertens. 1995;8:1–4. https://doi.org/10.1016/0895-7061(94)00166-9.
Joffe GM, et al. The relationship between abnormal glucose tolerance and hypertensive disorders of pregnancy in healthy nulliparous women. Calcium for Preeclampsia Prevention (CPEP) Study Group. Am J Obstet Gynecol. 1998;179:1032–7.
Wolf M, et al. First trimester insulin resistance and subsequent preeclampsia: a prospective study. J Clin Endocrinol Metab. 2002;87:1563–8. https://doi.org/10.1210/jcem.87.4.8405.
Parretti E, et al. Preeclampsia in lean normotensive normotolerant pregnant women can be predicted by simple insulin sensitivity indexes. Hypertension. 2006;47:449–53. https://doi.org/10.1161/01.HYP.0000205122.47333.7f.
Matthews DR, et al. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28:412–9.
Kirwan JP, Huston-Presley L, Kalhan SC, Catalano PM. Clinically useful estimates of insulin sensitivity during pregnancy: validation studies in women with normal glucose tolerance and gestational diabetes mellitus. Diabetes Care. 2001;24:1602–7.
Hauth JC, et al. Maternal insulin resistance and preeclampsia. Am J Obstet Gynecol. 2011;204(327):e321–6. https://doi.org/10.1016/j.ajog.2011.02.024.
D’Anna R, et al. Adiponectin and insulin resistance in early- and late-onset pre-eclampsia. BJOG. 2006;113:1264–9. https://doi.org/10.1111/j.1471-0528.2006.01078.x.
Montoro MN, et al. Insulin resistance and preeclampsia in gestational diabetes mellitus. Diabetes Care. 2005;28:1995–2000.
Sierra-Laguado J, et al. Determination of insulin resistance using the homeostatic model assessment (HOMA) and its relation with the risk of developing pregnancy-induced hypertension. Am J Hypertens. 2007;20:437–42. https://doi.org/10.1016/j.amjhyper.2006.10.009.
Legro RS. Insulin resistance in women’s health: why it matters and how to identify it. Curr Opin Obstet Gynecol. 2009;21:301–5. https://doi.org/10.1097/GCO.0b013e32832e07d5.
Ryan EA, et al. Defects in insulin secretion and action in women with a history of gestational diabetes. Diabetes. 1995;44:506–12.
Fuh MM, et al. Resistance to insulin-mediated glucose uptake and hyperinsulinemia in women who had preeclampsia during pregnancy. Am J Hypertens. 1995;8:768–71.
Soonthornpun K, Soonthornpun S, Wannaro P, Setasuban W, Thamprasit A. Insulin resistance in women with a history of severe pre-eclampsia. J Obstet Gynaecol Res. 2009;35:55–9. https://doi.org/10.1111/j.1447-0756.2008.00865.x.
Sattar N, Ramsay J, Crawford L, Cheyne H, Greer IA. Classic and novel risk factor parameters in women with a history of preeclampsia. Hypertension. 2003;42:39–42. https://doi.org/10.1161/01.HYP.0000074428.11168.EE.
Girouard J, Giguere Y, Moutquin JM, Forest JC. Previous hypertensive disease of pregnancy is associated with alterations of markers of insulin resistance. Hypertension. 2007;49:1056–62. https://doi.org/10.1161/HYPERTENSIONAHA.107.087528.
Smith GN, et al. A history of preeclampsia identifies women who have underlying cardiovascular risk factors. Am J Obstet Gynecol. 2009;200:58.e1–8. https://doi.org/10.1016/j.ajog.2008.06.035.
Agatisa PK, et al. Impairment of endothelial function in women with a history of preeclampsia: an indicator of cardiovascular risk. Am J Physiol Heart Circ Physiol. 2004;286:H1389–93. https://doi.org/10.1152/ajpheart.00298.2003.
Kvehaugen AS, et al. Endothelial function and circulating biomarkers are disturbed in women and children after preeclampsia. Hypertension. 2011;58:63–9. https://doi.org/10.1161/HYPERTENSIONAHA.111.172387.
Hawfield A, Freedman BI. Pre-eclampsia: the pivotal role of the placenta in its pathophysiology and markers for early detection. Ther Adv Cardiovasc Dis. 2009;3:65–73. https://doi.org/10.1177/1753944708097114.
Caballero AE. Endothelial dysfunction, inflammation, and insulin resistance: a focus on subjects at risk for type 2 diabetes. Curr Diab Rep. 2004;4:237–46.
Callaway LK, et al. Diabetes mellitus in the 21 years after a pregnancy that was complicated by hypertension: findings from a prospective cohort study. Am J Obstet Gynecol. 2007;197(492):e491–7. https://doi.org/10.1016/j.ajog.2007.03.033.
Lykke JA, et al. Hypertensive pregnancy disorders and subsequent cardiovascular morbidity and type 2 diabetes mellitus in the mother. Hypertension. 2009;53:944–51. https://doi.org/10.1161/HYPERTENSIONAHA.109.130765.
Engeland A, et al. Risk of diabetes after gestational diabetes and preeclampsia. A registry-based study of 230,000 women in Norway. Eur J Epidemiol. 2011;26:157–63. https://doi.org/10.1007/s10654-010-9527-4.
Feig DS, et al. Preeclampsia as a risk factor for diabetes: a population-based cohort study. PLoS Med. 2013;10:e1001425. https://doi.org/10.1371/journal.pmed.1001425.
Facca TA, Kirsztajn GM, Sass N. Preeclampsia (marker of chronic kidney disease): from genesis to future risks. J Bras Nefrol. 2012;34:87–93.
Craici I, Wagner S, Garovic VD. Preeclampsia and future cardiovascular risk: formal risk factor or failed stress test? Ther Adv Cardiovasc Dis. 2008;2:249–59. https://doi.org/10.1177/1753944708094227.
Harskamp RE, Zeeman GG. Preeclampsia: at risk for remote cardiovascular disease. Am J Med Sci. 2007;334:291–5. https://doi.org/10.1097/MAJ.0b013e3180a6f094.
Kanasaki K, Kalluri R. The biology of preeclampsia. Kidney Int. 2009;76:831–7.
Kanasaki K, et al. Deficiency in catechol-O-methyltransferase and 2-methoxyoestradiol is associated with pre-eclampsia. Nature. 2008;453:1117–21. https://doi.org/10.1038/nature06951.
Tunbridge EM, Harrison PJ, Weinberger DR. Catechol-o-methyltransferase, cognition, and psychosis: Val158Met and beyond. Biol Psychiatry. 2006;60:141–51.
Barnea ER, MacLusky NJ, DeCherney AH, Naftolin F. Catechol-o-methyl transferase activity in the human term placenta. Am J Perinatol. 1988;5:121–7.
Yan J, et al. 2-methoxyestradiol reduces cerebral vasospasm after 48 hours of experimental subarachnoid hemorrhage in rats. Exp Neurol. 2006;202:348–56.
Barchiesi F, et al. 2-Methoxyestradiol, an estradiol metabolite, inhibits neointima formation and smooth muscle cell growth via double blockade of the cell cycle. Circ Res. 2006;99:266–74. https://doi.org/10.1161/01.RES.0000233318.85181.2e.
Dubey RK, Jackson EK, Keller PJ, Imthurn B, Rosselli M. Estradiol metabolites inhibit endothelin synthesis by an estrogen receptor-independent mechanism. Hypertension. 2001;37:640–4.
Dubey RK, Jackson EK. Potential vascular actions of 2-methoxyestradiol. Trends Endocrinol Metab. 2009;20:374–9. https://doi.org/10.1016/j.tem.2009.04.007.
Lee SB, et al. Preeclampsia: 2-methoxyestradiol induces cytotrophoblast invasion and vascular development specifically under hypoxic conditions. Am J Pathol. 2010;176:710–20.
Takanashi K, Honma T, Kashiwagi T, Honjo H, Yoshizawa I. Detection and measurement of urinary 2-hydroxyestradiol 17-sulfate, a potential placental antioxidant during pregnancy. Clin Chem. 2000;46:373–8.
Annerbrink K, et al. Catechol O-methyltransferase val158-met polymorphism is associated with abdominal obesity and blood pressure in men. Metabolism. 2008;57:708–11.
Zhu BT. Catechol-O-Methyltransferase (COMT)-mediated methylation metabolism of endogenous bioactive catechols and modulation by endobiotics and xenobiotics: importance in pathophysiology and pathogenesis. Curr Drug Metab. 2002;3:321–49.
Need AC, Ahmadi KR, Spector TD, Goldstein DB. Obesity is associated with genetic variants that alter dopamine availability. Ann Hum Genet. 2006;70:293–303. https://doi.org/10.1111/j.1529-8817.2005.00228.x.
Tworoger SS, et al. The effect of CYP19 and COMT polymorphisms on exercise-induced fat loss in postmenopausal women. Obes Res. 2004;12:972–81.
Hall KT, et al. Catechol-O-methyltransferase association with hemoglobin A1c. Metabolism. 2016;65:961–7. https://doi.org/10.1016/j.metabol.2016.04.001.
Barchiesi F, et al. Candidate genes and mechanisms for 2-methoxyestradiol-mediated vasoprotection. Hypertension. 2010;56:964–72. https://doi.org/10.1161/HYPERTENSIONAHA.110.152298.
Matthews L, et al. Thiazolidinediones are partial agonists for the glucocorticoid receptor. Endocrinology. 2009;150:75–86. https://doi.org/10.1210/en.2008-0196.
Waite LL, et al. Placental peroxisome proliferator-activated receptor-gamma is up-regulated by pregnancy serum. J Clin Endocrinol Metab. 2000;85:3808–14. https://doi.org/10.1210/jcem.85.10.6847.
Waite LL, Louie RE, Taylor RN. Circulating activators of peroxisome proliferator-activated receptors are reduced in preeclamptic pregnancy. J Clin Endocrinol Metab. 2005;90:620–6. https://doi.org/10.1210/jc.2004-0849.
Barroso I, et al. Dominant negative mutations in human PPARgamma associated with severe insulin resistance, diabetes mellitus and hypertension. Nature. 1999;402:880–3. https://doi.org/10.1038/47254.
Ueki N, Kanasaki K, Kanasaki M, Takeda S, Koya D. Catechol-O-methyltransferase deficiency leads to hypersensitivity of the pressor response against angiotensin II. Hypertension. 2017;69:1156–64. https://doi.org/10.1161/HYPERTENSIONAHA.117.09247.
Berg D, Sonsalla R, Kuss E. Concentrations of 2-methoxyoestrogens in human serum measured by a heterologous immunoassay with an 125I-labelled ligand. Acta Endocrinol (Copenh). 1983;103:282–8.
Kanasaki M, et al. Deficiency in catechol-o-methyltransferase is linked to a disruption of glucose homeostasis in mice. Sci Rep. 2017;7:7927.
Coletta DK, et al. Pioglitazone stimulates AMP-activated protein kinase signalling and increases the expression of genes involved in adiponectin signalling, mitochondrial function and fat oxidation in human skeletal muscle in vivo: a randomised trial. Diabetologia. 2009;52:723–32. https://doi.org/10.1007/s00125-008-1256-9.
Acknowledgments
The author declares no conflicts of interests related to this work. This work was partially supported by grants from the Japan Society for the Promotion of Science for KK (23790381, 26460403) and several research grants for KK (the Daiichi-Sankyo Foundation of Life Science, the Ono Medical Research Foundation, the Takeda Science Foundation, Novo Nordisk Insulin Research Foundation, and the Banyu Life Science Foundation International). This work was partially supported by Grant for Promoted Research awarded to KK (S2014-4, S2015-3, S2016-3, S2017-1) from Kanazawa Medical University. This work was also partially supported by the Medical Research Encouragement Prize of the Japan Medical Association for KK. Boehringer Ingelheim (Japan), Mitsubishi Tanabe Pharma, and Ono Pharmaceutical contributed to establishing the Division of Anticipatory Molecular Food Science and Technology. KK is under a consultancy agreement with Boehringer Ingelheim.
Author information
Authors and Affiliations
Corresponding author
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2018 Springer Nature Singapore Pte Ltd.
About this chapter
Cite this chapter
Kanasaki, K. (2018). Glucose Intolerance and Insulin Resistance: Relevance in Preeclampsia. In: Saito, S. (eds) Preeclampsia. Comprehensive Gynecology and Obstetrics. Springer, Singapore. https://doi.org/10.1007/978-981-10-5891-2_5
Download citation
DOI: https://doi.org/10.1007/978-981-10-5891-2_5
Published:
Publisher Name: Springer, Singapore
Print ISBN: 978-981-10-5890-5
Online ISBN: 978-981-10-5891-2
eBook Packages: MedicineMedicine (R0)