Blunted glucose metabolism in anorexia nervosa

Only few studies have specifically investigated diet-induced thermogenesis in anorexia nervosa. Twenty women, 10 anorectics (body mass index [BMI] = 1 4.98 +/-1.02 kg/m(2)) and 10 controls (BMI = 22.53 +/-0.75 kg/m(2)) were st udied. Body composition was evaluated by isotopic dilution. Respiratory gas exchange was measured by indirect calorimetry. An oral glucose load (75 g) was administered to the anorectics (A) and the controls (CA). The controls underwent a second load (CB) with a higher glucose amount (1.85 +/-0.11 g/ kg body weight [BW]) to compare with the load taken by anorectics. Glucose- induced thermogenesis (GIT) was computed for 300 minutes following the load as the percent increase of energy expenditure (EE) above resting-EE (REE). Serum glucose levels were lower in anorectic patients both in fasting (3.4 6 +/-0.66 v 5.23 +/-0.23 in CA, P<.01 v 5.32<plus/minus>0.34 mmol in CB, P< .01) and in the postprandial state (glucose area under the curve [AUC] 175. 51<plus/minus>6.40 v 289.80 +/-7.30 in CA, P<.01 v 324.65 mmol in CB, P<.00 1); insulin AUG was lower, 1,926 +/- 452 versus 41,148 +/-2,071 in CA, P<.0 001 versus 60,765.5 pmol in CB, P<.0001. REE, normalized by fat-free mass ( FFM), was similar between groups. GIT was lower in anorectics (3.58 +/-1.20 v 5.45 +/-1.83 in CA, P<.05 v 9.09%<plus/minus>1.05% in CB, P<.01). Glucos e oxidation was higher in anorectics than in CA (689.44<plus/minus>72.22 v 333.32 +/- 32.98 mu mol/L/min, P<.001), but similar to CB. Lipid oxidation become negative after 30 minutes in anorectics (postprandial lipid oxidatio n = -93.58<plus/minus>39.86 v 370.61 +/- 21.73 in CA, P<.0001 v 119.01 <plu s/minus> 12.32 mu mol/L/300 min in CB, P <.0001). Anorectic patients displa yed a low REE and GIT. Carbohydrate oxidation was similar between groups; l ipid oxidation was extremely reduced. An increased protein catabolism was o bserved. Copyright (C) 2001 by W.B. Saunders Company.