title: Acute pain induces insulin resistance in humans.
abstract: BACKGROUND
  Painful trauma results in a disturbed metabolic state with impaired insulin sensitivity, which is related to the magnitude of the trauma. The authors explored whether pain per se influences hepatic and extrahepatic actions of insulin.
  
  
  METHODS
  Ten healthy male volunteers underwent two randomly sequenced hyperinsulinemic-euglycemic (insulin infusion rate, 0.6 mU x kg(-1) x min(-1) for 180 min) clamp studies 4 weeks apart. Self-controlled painful electrical stimulation was applied to the abdominal skin for 30 min, to a pain intensity of 8 on a visual analog scale of 0-10, just before the clamp procedure (study P). In the other study, no pain was inflicted (study C).
  
  
  RESULTS
  Pain reduced whole-body insulin-stimulated glucose uptake from 6.37+/-1.87 mg x kg(-1) x min(-1) (mean +/- SD) in study C to 4.97+/-1.38 mg x kg(-1) x min(-1) in study P (P < 0.01) because of a decrease in nonoxidative glucose disposal, as determined by indirect calorimetry (2.47+/-0.88 mg x kg(-1) x min(-1) in study P vs. 3.41+/-1.03 mg x kg(-1) x min(-1) in study C; P < 0.05). Differences in glucose oxidation rates were not statistically significant. The suppression of isotopically determined endogenous glucose output during hyperinsulinemia tended to be decreased after pain (1.67+/-0.48 mg x kg(-1) x min(-1) in study P vs. 2.04+/-0.45 mg x kg(-1) x min(-1) in study C; P = 0.06). Pain elicited a twofold to threefold increase in serum cortisol (P < 0.01), plasma epinephrine (P < 0.05), and serum free fatty acids (P < 0.05). Similarly, circulating concentrations of glucagon and growth hormone tended to increase during pain.
  
  
  CONCLUSIONS
  Acute severe pain decreases insulin sensitivity, primarily by affecting nonoxidative glucose metabolism. It is conceivable that the counterregulatory hormonal response plays an important role. This may indicate that pain relief in stress states is important for maintenance of normal glucose metabolism.
authors.affiliation: Department of Medicine V and Center for Clinical Pharmacology, Aarhus University Hospital, Denmark. jg@farm.au.dk
authors.forename: J
authors.initials: J
authors.lastname: Greisen
authors.forename: C B
authors.initials: CB
authors.lastname: Juhl
authors.forename: T
authors.initials: T
authors.lastname: Grøfte
authors.forename: H
authors.initials: H
authors.lastname: Vilstrup
authors.forename: T S
authors.initials: TS
authors.lastname: Jensen
authors.forename: O
authors.initials: O
authors.lastname: Schmitz
mesh_terms: D000208:Acute Disease; D000328:Adult; D002395:Catecholamines / Q000097:blood; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005947:Glucose / Q000378:metabolism; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008297:Male; D010146:Pain / Q000378:metabolism*
chemical_list: D002395:Catecholamines; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D005947:Glucose; D006854:Hydrocortisone