Animal models for assessing the consequences of intrauterine growth restriction on subsequent glucose metabolism of the offspring: a review.
OBJECTIVE
The aim of this article was to review the most current animal models for intrauterine growth restriction.


METHODS
The databases of MEDLINE and Pubmed were searched for articles published between 1969 and 2001. Additional sources included abstract proceedings and relevant reference lists of articles identified by database review. Key words included intrauterine growth retardation, small for gestational age, animal models and glucose metabolism. The inclusion criteria used to select studies included animal models of intrauterine growth retardation in which glucose metabolism was assessed after birth.


RESULTS
A variety of physiological and metabolic variables regulate fetal growth, and alteration of these variables can result in fetal growth restriction. Fetal growth restriction is secondary to initiation of fetal adaptation measures in response to inadequate supply of oxygen and nutrients. Several animal models have led to a greater understanding of the pathophysiology and consequences of intrauterine growth restriction. These observations are comparable to those observed in humans born small for gestational age, and are of interest because of the known association between poor fetal growth and development of glucose intolerance and type 2 diabetes mellitus later in life.


CONCLUSIONS
Experimental manipulations have apparently altered a number of metabolic and physiological variables, but the pattern of alterations seems to vary with the procedure employed. This allows only a preliminary conclusion to be drawn at best. Either the laboratory procedures vitiate the natural process under study, or the process itself is variable with respect to the triggering mechanism. As yet, we cannot tell which.
Vuguin
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Pediatric Endocrinology, Children's Hospital at Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, New York, USA.
D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology* / Q000503:physiopathology; D005260:Female; D005317:Fetal Growth Retardation / Q000150:complications* / Q000503:physiopathology; D005947:Glucose / Q000378:metabolism*; D018149:Glucose Intolerance / Q000209:etiology* / Q000503:physiopathology; D006801:Humans; D023421:Models, Animal; D010927:Placental Insufficiency / Q000150:complications; D011247:Pregnancy; D011254:Pregnancy in Diabetics / Q000503:physiopathology*; D039401:Prenatal Nutritional Physiological Phenomena / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar
D005947:Glucose