GLUCOSE-TURNOVER IN LEAN AND OBESE RATS OF THE SHR N-CP AND LA/N-CP STRAINS/

Citation
Cd. Berdanier et al., GLUCOSE-TURNOVER IN LEAN AND OBESE RATS OF THE SHR N-CP AND LA/N-CP STRAINS/, Comparative biochemistry and physiology. B. Comparative biochemistry, 106(1), 1993, pp. 87-94
Citations number
40
Categorie Soggetti
Biology
ISSN journal
03050491
Volume
106
Issue
1
Year of publication
1993
Pages
87 - 94
Database
ISI
SICI code
0305-0491(1993)106:1<87:GILAOR>2.0.ZU;2-B
Abstract
1. The relationship between hypertension, obesity, non-insulin-depende nt diabetes mellitus and various parameters of glucose metabolism was studied. Lean and obese rats of the SHR/N-cp and LA/N-cp congenic stra ins were studied at four months of age. 2. Tritium and C-14-labeled gl ucoses were infused in one set of rats while tritiated water and C-14- labeled alanine were infused in a second group. 3. Glucose oxidation, turnover, conversion to glycogen, fatty acid synthesis, and alanine co nversion to glucose were determined, as were blood pressure, pulse pre ssure and heart rate. 4. The presence of obesity influenced body weigh t, body fat, de novo fatty acid synthesis, organ weights, glucose mass , glurose oxidation, glucose synthesis, glucose carbon turnover and pu lse pressure. 5. It had no effect on glycogen synthesis, tissue glycog en levels, blood glucose, glucose space, or blood pressure. 6. Strain differences were observed in final body weight, organ weights, blood p ressure, pulse pressure, hepatic fatty acid synthesis, glucose mass, g lucose space, glucose synthesis, liver glycogen levels and glucose con version to muscle glycogen. 7. Strain-phenotype interaction effects we re observed on glucose incorporation into hepatic glycogen, Cori cycle activity, hepatic de novo fatty acid synthesis, final body weight, fa t pad weight, heart weight, and mean arterial pressure. 8. These resul ts suggest that although obesity and hypertension are genetic traits i n these rats, these traits are independent in their influence on the m etabolism of glucose and the development of non-insulin-dependent diab etes mellitus.