PROTEIN AND GLUCOSE-METABOLISM DURING ISOLATED CLOSED-HEAD INJURY

Citation
Pj. Flakoll et al., PROTEIN AND GLUCOSE-METABOLISM DURING ISOLATED CLOSED-HEAD INJURY, American journal of physiology: endocrinology and metabolism, 32(4), 1995, pp. 636-641
Citations number
37
Categorie Soggetti
Physiology
ISSN journal
01931849
Volume
32
Issue
4
Year of publication
1995
Pages
636 - 641
Database
ISI
SICI code
0193-1849(1995)32:4<636:PAGDIC>2.0.ZU;2-J
Abstract
Patients with isolated closed-head injuries are characterized by exces sive nitrogen loss, hyperglycemia, and increased caloric demand. Howev er, the relative contributions of specific metabolic events such as pr otein breakdown and synthesis or glucose production and utilization to the physiological changes prevalent during isolated closed-head injur y remains unestablished. By use of isotopic dilutions of L-[1-C-13]leu cine and D-[3-H-3]glucose, components of protein and glucose metabolis m were examined in patients with isolated closed-head injury (n = 7). Normal overnight-fasted volunteers (n = 8) were also studied as a refe rence point for comparison. Despite prevailing hyperinsulinemia (29 +/ - 5 mu U/ml), head-injured patients had elevated plasma leucine concen trations (183 +/- 22 vs. 144 +/- 8 mu mol/l), whole body proteolysis ( 331 +/- 44 vs. 150 +/- 7 mg . kg(-1). h(-1)), protein synthesis (248 /- 38 vs. 126 +/- 11 mg . kg(-1). h(-1)), and amino acid oxidation (84 +/- 11 vs. 23 +/- 3 mg . kg(-1). h(-1)). Therefore nitrogen loss norm ally associated with isolated closed-head injury is primarily due to a n increase in the rate of whole body proteolysis, with a greater propo rtion of the resultant amino acids being oxidized for energy. Furtherm ore, head-injured patients were hyperglycemic (6.7 +/- 0.3 mu mol/l) w ith increased rates of glucose turnover (an estimate of production and utilization) compared with the controls (4.0 +/- 0.7 vs. 2.5 +/- 0.2 mg . kg(-1). min(-1)). Hence, these data suggest that head injury, eve n in the absence of peripheral trauma, induces a physiological state o f accelerated metabolism associated with resistance to insulin action.