Fibrinogen kinetics and protein turnover in obese non-diabetic males: effects of insulin
Article first published online: 26 NOV 2009
Copyright © 2009 John Wiley & Sons, Ltd.
Diabetes/Metabolism Research and Reviews
Volume 26, Issue 1, pages 50–58, January 2010
How to Cite
Tessari, P., Cosma, A., Vettore, M., Millioni, R., Puricelli, L., Cogo, P., Cecchet, D., Carnielli, V. and Kiwanuka, E. (2010), Fibrinogen kinetics and protein turnover in obese non-diabetic males: effects of insulin. Diabetes Metab. Res. Rev., 26: 50–58. doi: 10.1002/dmrr.1055
- Issue published online: 25 JAN 2010
- Article first published online: 26 NOV 2009
- Manuscript Accepted: 26 OCT 2009
- Manuscript Revised: 7 OCT 2009
- Manuscript Received: 3 DEC 2008
- University of Padova
- Italian Ministry of Education, University and Research
- ‘Fondazione Cassa di Risparmio di Padova e Rovigo’
- insulin sensitivity;
- fibrinogen FSR and ASR;
- stable isotopes;
- euglycemic clamp;
- amino acid clearance
Although hyperfibrinogenemia and insulin resistance are common in obesity and diabetes mellitus, the impact of obesity per se on fibrinogen turnover and the insulin effects on fibrinogen and protein kinetics is unknown.
We measured fibrinogen and albumin fractional (FSR) and absolute (ASR) synthesis rates, as well as protein turnover, in non-diabetic, obese and in control male subjects both before and following an euglycemic, euaminoacidemic, hyperinsulinemic clamp, using L-[2H3]-Leucine isotope infusion.
In the obese, basal fibrinogen concentrations was ≈ 25% greater (p < 0.035), and fibrinogen pool ≈ 45% greater (p < 0.005), than in controls. Both FSR and ASR of fibrinogen were similar to control values. With hyperinsulinemia, although fibrinogen FSR and ASR were not significantly modified with respect to baseline in either group, fibrinogen ASR resulted to be ≈ 50% greater in the obese than in controls (p < 0.015). Hyperinsulinemia equally stimulated albumin synthesis and suppressed leucine appearance from endogenous proteolysis in both groups. Amino acid clearance was also similar. In the obese, the insulin-mediated glucose disposal was ≈ 50% lower (p < 0.03) than in controls, and it was inversely correlated with fibrinogen ASR during the clamp in both groups (r = − 0.58).
In obese, non-diabetic males, post absorptive fibrinogen production is normal. Whole-body amino acid disposal, basal and insulin-responsive protein degradation, and albumin synthesis are also normal. However, the greater fibrinogen ASR in the obese with hyperinsulinemia, and the inverse relationship between insulin sensitivity and clamp fibrinogen production, suggest a role for hyperinsulinemia and/or insulin resistance on fibrinogen production in obesity. Copyright © 2009 John Wiley & Sons, Ltd.