GLUCOSE-INDUCED THERMOGENESIS IN TETRAPLEGIC PATIENTS WITH LOW SYMPATHOADRENAL ACTIVITY

The influence of the sympathoadrenal system on the thermic effect of glucose was examined by studying six tetraplegic patients with complete lesions of the cervical spinal cord. Indirect calorimetry and catheter techniques were employed, and measurements were made before and during 2 h after oral ingestion of 75 g of glucose. The results were compared with previous findings from an identical study in healthy subjects and with those from a control group of five tetraplegic patients receiving water instead of glucose. In response to glucose, energy expenditure rose from 69 +/- 5 to 79 +/- 5 and from 88 +/- 3 to 98 +/- 4 W, (not significant) in the patients and healthy subjects, respectively. In both patients and the healthy subjects the postprandial oxygen consumption increased exclusively in extrasplanchnic tissues. Splanchnic blood flow, which in normals increased 34 +/- 1%, did not change in the patients after glucose. Blood temperatures were unchanged in normals after glucose but rose by similar to 0.5 degrees C in the patients. The patients' arterial plasma concentrations of norepinephrine were low in the basal state and did not rise significantly after glucose. The arterial blood glucose concentrations after glucose were significantly higher in the patients than in the healthy subjects. Insulin levels rose to 105 +/- 20 mU/l in the patients and to 59 +/- 7 mU/l in the controls (P < 0.02). The postprandial splanchnic release of glucose was similar in patients and healthy subjects, whereas the simultaneous splanchnic release of insulin was in the patients only one-third of that in normals (P < 0.05). It is concluded that 1) an intact sympathetic nervous system is not required for a normal thermic effect of glucose, 2) the glucose-induced rise in splanchnic blood flow is in part mediated via the sympathetic nervous system, 3) glucose ingestion causes heat accumulation in tetraplegic patients but not in normal humans, and 4) the rate of insulin catabolism is reduced in tetraplegic patients.