اثر افزایش وزن ناشی از درمانی بر روی میزان لپتین پلاسما در بیماران مبتلا به بی اشتهایی عصبی
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|33722||2003||5 صفحه PDF||سفارش دهید||2867 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Journal of Psychiatric Research, Volume 37, Issue 2, March–April 2003, Pages 165–169
Previously it was shown that hyperleptinemia ensues from the therapeutically induced weight gain in patients with anorexia nervosa (AN). However, not all studies have been able to confirm this finding. To further investigate leptin secretion during weight gain in AN and potential functional implications serum leptin levels, body mass index (BMI),% body fat, fT3, fT4 and TSH of 18 adolescent AN patients (BMI at admission: 14.4±1.2) were examined four times during 11 weeks of re-feeding and compared to 18 weight stable controls. Additionally, serum leptin levels, BMI and % body fat were determined in patients reaching target weight after 11–20 weeks (mean 14.3±3) of inpatient re-feeding. At admission patients showed lower lg10 leptin levels (P=0.000) and BMI (P=0.000) than controls. At target weight patients still had significantly lower BMI (P=0.000) and% body fat (P=0.000) than controls but lg10 leptin levels of patients were higher than those of controls when adjusted for BMI and% body fat (ANCOVA, group P=0.038). In patients, correlation coefficients between lg10 leptin levels and BMI increments increased during the 11 weeks of re-feeding. BMI,% body fat and fT3 levels were not significantly correlated to lg10 leptin levels in week 11, however, 53% of the variance of leptin levels (corrected R2=0.53, P=0.001) was explained by BMI increments between weeks 7 and 11 (P=0.001) and lg10 leptin level at admission (P=0.002). In conclusion, we confirmed weight gain induced hyperleptinemia in AN. Further research is required to assess if this phenomenon contributes to renewed weight loss.
Anorexia nervosa (AN) is a psychiatric disorder with a high mortality. Re-feeding therapies are efficient in weight rehabilitation but rates of short-term relapses are nevertheless high (Herpertz-Dahlmann et al., 2001). Whereas there is no evidence to support the occurrence of a specific disturbance of the leptin system in AN (Ferron et al., 1997, Hebebrand et al., 1995, Hebebrand et al., 1997 and Hinney et al., 1998) temporary adaptive changes of leptin concentrations possibly interfere with weight stabilisation during or shortly after re-feeding therapies. Hebebrand et al., (1997) and Mantzoros et al. (1997) found reduced concentrations of the adipocyte hormone leptin during the acute stage of AN and increased levels upon short-term weight restoration compared to age-matched normal-weight controls. In contrast, two studies reported on decreased serum leptin levels in anorectic patients after partial weight recovery in contrast to normal weight controls (Casanueva et al., 1997 and Haluzik et al., 1999). Leptin plays an important role in the hypothalamic regulation of food intake and energy homeostasis. In lean and obese humans (Heymsfield et al., 1999) and in genetically leptin-deficient obese and wild type animals (van Dijk, 2001) leptin administration leads to a loss of weight and fat. Weight loss is presumably promoted by a reduction of food intake, an increase in energy expenditure, thermogenesis and degradation of fat stores (van Dijk, 2001). Thus, it is tempting to hypothesise that elevated leptin levels in AN patients during re-feeding may be an important factor in the difficulties of reaching or maintaining target-weight (Hebebrand et al., 1997). The aim of this study was to confirm elevated leptin secretion upon weight gain and to attempt to identify factors contributing to transient hyperleptinemia in AN during re-feeding.