title: Suboptimal protein nutrition in early life later influences insulin action in pregnant rats.
abstract: First-generation rats received either 20% (standard) or 8% (suboptimal) protein nutrition during pregnancy and lactation. Suboptimal protein nutrition led to reduced body weights of the second-generation progeny at day 19 of gestation (10%, p < 0.001) and at weaning (33% reduction, p < 0.001). Control (born of 20% protein-fed dams) and experimental (born of 8% protein-fed dams) offspring received 20% protein diet after weaning and were studied on day 19 of gestation at 9 to 12 weeks after weaning. Basal glucose turnover was lower (29%, p < 0.05) and glucose utilization by fast-twitch muscle, adipose tissue and diaphragm significantly reduced in experimental offspring. Hyperinsulinaemia increased whole-body glucose disposal rate in both control (2.3-fold, p < 0.001) and experimental (3.2-fold, p < 0.001) offspring. Hyperinsulinaemia normalised the suppression of glucose utilization observed in diaphragm, heart and adipose tissue, but not in fast-twitch muscle, where rates remained 30-40% lower in the experimental offspring. Glucose tolerance and insulin secretion after i.v. glucose were unimpaired in the pregnant experimental offspring. A 27% reduction in basal glucose utilization, without impaired growth, was observed for the third-generation fetuses of the experimental offspring. The results demonstrate that growth retardation evoked by suboptimal protein nutrition during early life leads to decreased basal glucose turnover and glucose utilization by a range of maternal tissues and the fetus during a subsequent pregnancy. It is not, however, associated with any major permanent impairment of glucose-stimulated insulin secretion or insulin action during pregnancy.
authors.affiliation: Department of Biochemistry, University of London, UK.
authors.forename: M J
authors.initials: MJ
authors.lastname: Holness
authors.forename: M C
authors.initials: MC
authors.lastname: Sugden
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000375:Aging; D000704:Analysis of Variance; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D005314:Embryonic and Fetal Development; D005260:Female; D005947:Glucose / Q000378:metabolism*; D006946:Hyperinsulinism; D007328:Insulin / Q000097:blood; D018656:Muscle Fibers, Fast-Twitch / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism; D009929:Organ Size; D010920:Placenta / Q000033:anatomy & histology / Q000502:physiology*; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000502:physiology*; D011502:Protein-Energy Malnutrition / Q000503:physiopathology*; D051381:Rats; D012016:Reference Values; D015430:Weight Gain
chemical_list: D001786:Blood Glucose; D007328:Insulin; D005947:Glucose