ECE2008 Poster Presentations Obesity (94 abstracts)
Medical University of Bialystok, Bialystok, Poland.
Anorexia nervosa (AN) is an eating disorder, with the significant loss of the adipose tissue. Lack of subcutaneous adipose tissue observed in lipodystrophies is accompanied by insulin resistance. The crucial step in the development of insulin resistance is an impaired increase in carbohydrate oxidation and decrease in lipid oxidation in response to insulin. The aim of the present study was to estimate carbohydrate and lipid oxidation in relation to serum adiponectin concentration in women with AN.
We examined 16 women with AN, 15 lean control women and 15 obese women. Euglycemic hyperinsulinemic clamp, indirect calorimetry in baseline state and during the last 30 min of the clamp and the measurements of serum adiponectin concentration were performed.
Insulin sensitivity was decreased in obese women in comparison to AN (P=0.0045) and controls (P=0.015), whereas it was not different between AN and controls. Serum adiponectin was higher in AN women in comparison to other groups (control, P=0.015; obese, P=0.038) and in control in comparison to the obese women (P=0.047). Women with AN had preserved carbohydrate and lipid oxidation, and non-oxidative glucose metabolism during hyperinsulinemia. All these parameters were not significantly differ from control group, although lipid oxidation in the hyperinsulinemic state tended to be lower in AN (P=0.066). Obese women had lower carbohydrate oxidation during the clamp in comparison to AN (P=0.022) and controls (P=0.01) and lower non-oxidative glucose metabolism and higher lipid oxidation during the clamp in comparison to AN (P=0.016 and P=0.038, respectively). Serum adiponectin was related to lipid oxidation during hyperinsulinemic state (r=−0.38, P=0.039).
Women with AN had normal insulin sensitivity due to the preserved response to insulin of substrate oxidation and non-oxidative glucose metabolism. Adiponectin is related to insulin sensitivity through its association with the suppression of lipid oxidation during hyperinsulinemia.