Suboptimal protein nutrition in early life later influences insulin action in pregnant rats

• Published in: Diabetologia 1996, Vol.39 (1), p.12-21
• Main Authors: HOLNESS, M. J, SUGDEN, M. C
• Format: Article
• Language: English
• Subjects: Adipose Tissue - metabolism; Aging; Analysis of Variance; Animals; Biological and medical sciences; Blood Glucose - metabolism; Body Weight; Diabetes. Impaired glucose tolerance; Embryonic and Fetal Development; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Etiopathogenesis. Screening. Investigations. Target tissue resistance; Female; Glucose - metabolism; Hyperinsulinism; Insulin - blood; Medical sciences; Muscle Fibers, Fast-Twitch - metabolism; Muscle, Skeletal - metabolism; Organ Size; Placenta - anatomy & histology; Placenta - physiology; Pregnancy; Pregnancy, Animal - physiology; Protein-Energy Malnutrition - physiopathology; Rats; Reference Values; Weight Gain
• ISSN: 0012-186X; 1432-0428
• DOI: 10.1007/BF00400408

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.