Acute pain induces insulin resistance in humans

Background Painful trauma results in a disturbed metabolic state with Impai red Insulin sensitivity, which is related to the magnitude of the trauma. T he authors explored whether pain per se Influences hepatic and extrahepatic actions of insulin. Methods: Ten healthy male volunteers underwent two randomly sequenced hyper insulinemic-euglycemic (Insulin infusion rate, 0.6 mU (.) kg(-1) (.) min(-1 ) for 180 min) clamp studies 4 weeks apart. Self-controlled painful electri cal stimulation was applied to the abdominal skin for 30 min, to a pain int ensity of 8 on a visual analog scale of 0-10, just before the clamp procedu re (study P). in the other study, no pain was inflicted (study C). Results: Pain reduced whole-body insulin-stimulated glucose uptake from 6.3 7 +/- 1.87 mg (.) kg(-1) (.) min(-1) (mean +/- SD) in study C to 4.97 +/- 1 .38 mg (.) kg(-1) (.) min(-1) In study P (P < 0.01) because of a decrease i n nonoxidative glucose disposal, as determined by indirect calorimetry (2.4 7 +/- 0.88 mg (.) kg(-1) (.) min(-1) in study P vs. 3.41 +/- 1.03 mg (.) kg (-1) (.) min(-1) in study C; P < 0.05). Differences in glucose oxidation ra tes were not statistically significant. The suppression of isotopically det ermined endogenous glucose output during hyperinsulinemia tended to be decr eased after pain (1.67 +/- 0.48 mg (.) kg(-1) (.) min(-1) in study P vs. 2. 04 +/- 0.45 mg (.) kg(-1) (.) min(-1) in study C; P = 0.06). Pain elicited a twofold to threefold increase in serum cortisol (P < 0.01), plasma epinep hrine (P < 0.05), and serum free fatty acids (P < 0.05). Similarly, circula ting concentrations of glucagon and growth hormone tended to increase durin g pain. Conclusions: Acute severe pain decreases insulin sensitivity, primarily by affecting nonoxidative glucose metabolism. It is conceivable that the count erregulatory hormonal response plays an Important role. This may indicate t hat pain relief in stress states is important for maintenance of normal glu cose metabolism.