Intrauterine Growth Restriction

Intrauterine Growth Restriction: Comparison

Please note this is a comparison between Version 2 by Vicky Zhou and Version 1 by Daniel Hardy.

Intrauterine growth restriction (IUGR), or fetal growth restriction, refers to poor growth of a fetus while in the womb during pregnancy. IUGR is defined by clinical features of malnutrition and evidence of reduced growth regardless of an infant's birth weight percentile. The causes of IUGR are broad and may involve maternal, fetal, or placental complications. At least 60% of the 4 million neonatal deaths that occur worldwide every year are associated with low birth weight (LBW), caused by intrauterine growth restriction (IUGR), preterm delivery, and genetic abnormalities, demonstrating that under-nutrition is already a leading health problem at birth. Intrauterine growth restriction can result in a baby being small for gestational age (SGA), which is most commonly defined as a weight below the 10th percentile for the gestational age. At the end of pregnancy, it can result in a low birth weight.

Intrauterine growth restriction (IUGR) is a pathological condition by which the fetus deviates from its expected growth trajectory, resulting in low birth weight and impaired organ function. The developmental origins of health and disease (DOHaD) postulates that IUGR has lifelong consequences on offspring well-being, as human studies have established an inverse relationship between birth weight and long-term metabolic health. While these trends are apparent in epidemiological data, animal studies have been essential in defining the molecular mechanisms that contribute to this relationship. One such mechanism is cellular stress, a prominent underlying cause of the metabolic syndrome.

intrauterine growth restriction (IUGR)
metabolism
cell stress
cell death
metabolic syndrome

Please wait, diff process is still running!

References

Ravelli, G.P.; Stein, Z.A.; Susser, M.W. Obesity in Young Men after Famine Exposure in Utero and Early Infancy. N. Engl. J. Med. 1976, 295, 349–353.
Ravelli, A.C.; van der Meulen, J.H.; Michels, R.P.; Osmond, C.; Barker, D.J.; Hales, C.N.; Bleker, O.P. Glucose Tolerance in Adults after Prenatal Exposure to Famine. Lancet 1998, 351, 173–177.
Ravelli, A.C.; van der Meulen, J.H.; Osmond, C.; Barker, D.J.; Bleker, O.P. Obesity at the Age of 50 y in Men and Women Exposed to Famine Prenatally. Am. J. Clin. Nutr. 1999, 70, 811–816.
Baschat, A.A. Pathophysiology of Fetal Growth Restriction: Implications for Diagnosis and Surveillance. Obstet. Gynecol. Surv. 2004, 59, 617–627.
Sharma, D.; Shastri, S.; Sharma, P. Intrauterine Growth Restriction: Antenatal and Postnatal Aspects. Clin. Med. Insights. Pediatrics 2016, 10, 67–83.
Barker, D.J.; Martyn, C.N.; Osmond, C.; Hales, C.N.; Fall, C.H. Growth in Utero and Serum Cholesterol Concentrations in Adult Life. BMJ 1993, 307, 1524–1527.
Hales, C.N.; Barker, D.J. The Thrifty Phenotype Hypothesis. Br. Med. Bull. 2001, 60, 5–20.
Kohnert, K.-D.; Freyse, E.-J.; Salzsieder, E. Glycaemic Variability and Pancreatic SS-Cell Dysfunction. Curr. Diabetes Rev. 2012, 8, 345–354.
Quan, W.; Jo, E.-K.; Lee, M.-S. Role of Pancreatic β -Cell Death and Inflammation in Diabetes. Diabetes Obes. Metab. 2013, 15, 141–151.
Saraste, A.; Pulkki, K.; Kallajoki, M.; Henriksen, K.; Parvinen, M.; Voipio-Pulkki, L.M. Apoptosis in Human Acute Myocardial Infarction. Circulation 1997, 95, 320–323.
Olivetti, G.; Quaini, F.; Sala, R.; Lagrasta, C.; Corradi, D.; Bonacina, E.; Gambert, S.R.; Cigola, E.; Anversa, P. Acute Myocardial Infarction in Humans Is Associated with Activation of Programmed Myocyte Cell Death in the Surviving Portion of the Heart. J. Mol. Cell. Cardiol. 1996, 28, 2005–2016.
Narula, J.; Haider, N.; Virmani, R.; DiSalvo, T.G.; Kolodgie, F.D.; Hajjar, R.J.; Schmidt, U.; Semigran, M.J.; Dec, G.W.; Khaw, B.-A. Apoptosis in Myocytes in End-Stage Heart Failure. N. Engl. J. Med. 1996, 335, 1182–1189.
Aharinejad, S.; Andrukhova, O.; Lucas, T.; Zuckermann, A.; Wieselthaler, G.; Wolner, E.; Grimm, M. Programmed Cell Death in Idiopathic Dilated Cardiomyopathy Is Mediated by Suppression of the Apoptosis Inhibitor Apollon. Ann. Thorac. Surg. 2008, 86, 109–114.
Muralimanoharan, S.; Li, C.; Nakayasu, E.S.; Casey, C.P.; Metz, T.O.; Nathanielsz, P.W.; Maloyan, A. Sexual Dimorphism in the Fetal Cardiac Response to Maternal Nutrient Restriction. J. Mol. Cell. Cardiol. 2017, 108, 181–193.
Iliescu, R.; Cucchiarelli, V.E.; Yanes, L.L.; Iles, J.W.; Reckelhoff, J.F. Impact of Androgen-Induced Oxidative Stress on Hypertension in Male SHR. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2007, 292, R731–R735.
Azhary, J.M.K.; Harada, M.; Takahashi, N.; Nose, E.; Kunitomi, C.; Koike, H.; Hirata, T.; Hirota, Y.; Koga, K.; Wada-Hiraike, O.; et al. Endoplasmic Reticulum Stress Activated by Androgen Enhances Apoptosis of Granulosa Cells via Induction of Death Receptor 5 in PCOS. Endocrinology 2019, 160, 119–132.
Jazwiec, P.A.; Patterson, V.S.; Ribeiro, T.A.; Yeo, E.; Kennedy, K.M.; Mathias, P.C.F.; Petrik, J.J.; Sloboda, D.M. Paternal Obesity Results in Placental Hypoxia and Sex-Specific Impairments in Placental Vascularization and Offspring Metabolic Function. bioRxiv 2021, preprint.
Raab, E.L.; Vuguin, P.M.; Stoffers, D.A.; Simmons, R.A. Neonatal Exendin-4 Treatment Reduces Oxidative Stress and Prevents Hepatic Insulin Resistance in Intrauterine Growth-Retarded Rats. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2009, 297, R1785–R1794.
Ozcan, U.; Yilmaz, E.; Ozcan, L.; Furuhashi, M.; Vaillancourt, E.; Smith, R.O.; Görgün, C.Z.; Hotamisligil, G.S. Chemical Chaperones Reduce ER Stress and Restore Glucose Homeostasis in a Mouse Model of Type 2 Diabetes. Science 2006, 313, 1137–1140.