Programming of impaired insulin secretion versus sensitivity: cause or effect?
A substantial body of evidence suggests that a poor intrauterine milieu elicited by maternal nutritional disturbance, including maternal diabetes or placental insufficiency, may programme susceptibility in the fetus to later development of glucose intolerance and diabetes. Numerous data in animals have allowed possible mechanisms for programming to be proposed. This review of work in several animal models attempts to identify the cellular and molecular mechanisms at the level of the beta-cell and in the insulin sensitive tissues that are involved in the process of events leading to the pathology later in life.
Reusens
Brigitte
B
Laboratoire de Biologie Cellulaire, Institut des Sciences de la Vie, Université catholique de Louvain, Louvain-la-Neuve, Belgique. reusens@bani.ucl.ac.be
Remacle
Claude
C
D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D018149:Glucose Intolerance / Q000378:metabolism*; D006801:Humans; D007223:Infant; D007227:Infant Nutritional Physiological Phenomena; D007231:Infant, Newborn; D007328:Insulin / Q000378:metabolism*; D008297:Male; D039382:Maternal Nutritional Physiological Phenomena; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000378:metabolism*; D039401:Prenatal Nutritional Physiological Phenomena; D051381:Rats
D007328:Insulin