Programming of hepatic and peripheral tissue insulin sensitivity by maternal protein restriction.
In recent years a great deal of research effort has been directed towards understanding the molecular basis of the relationship between markers of fetal and early growth retardation and the subsequent development of Type 2 diabetes. A lot of this work has focused on the maternal low protein rat model. Like many animal models, it does not perfectly represent the human situation and frank diabetes has not yet been produced. However, this model has yielded much information on potential mechanisms by which changes in insulin sensitivity can occur and has helped in understanding the role of the molecular machinery involved in the signalling of the metabolic actions of insulin.
Ozanne
S E
SE
Department of Clinical Biochemistry, University of Cambridge, U.K.
D000273:Adipose Tissue / Q000502:physiology; D000818:Animals; D001724:Birth Weight; D003924:Diabetes Mellitus, Type 2 / Q000209:etiology; D004044:Dietary Proteins / Q000008:administration & dosage; D005260:Female; D005317:Fetal Growth Retardation / Q000150:complications; D006801:Humans; D006973:Hypertension / Q000209:etiology; D007333:Insulin Resistance / Q000502:physiology*; D008099:Liver / Q000502:physiology*; D008297:Male; D008431:Maternal-Fetal Exchange / Q000502:physiology*; D009132:Muscles / Q000502:physiology; D017202:Myocardial Ischemia / Q000209:etiology; D010179:Pancreas / Q000502:physiology; D011247:Pregnancy; D051381:Rats
D004044:Dietary Proteins