کاهش غلظت لپتین پلاسما در بولیمیا
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|32477||2000||10 صفحه PDF||سفارش دهید||2261 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Psychoneuroendocrinology, Volume 25, Issue 7, October 2000, Pages 649–658
Leptin is a protein produced by the ob–ob gene which inhibits food intake. Plasma levels have previously been reported to be altered in obesity and anorexia nervosa (AN) but not bulimia nervosa (BN). We measured fasting plasma leptin levels by radioimmunoassay in 53 subjects carefully studied at NIMH, including 37 women meeting DSM–III–R criteria for BN [10 with concurrent AN (body mass index (BMI)=14.1±1.4), 27 without AN (BMI=20.4±1.6)] and 16 normal control women (NCs) (BMI=21.1±2.0). Patients were medication-free and abstinent from bingeing and purging for three to four weeks prior to study. Plasma leptin levels were significantly correlated to BMI (r=0.41, P<0.002), weight (kg, r=0.43, P<0.001), and percent average body weight (%ABW, r=0.45, P<0.001) in the total group. Plasma leptin levels were lower in the BN subjects (3.4±2.5 ng/ml) compared to the NCs (6.1±2.6 ng/ml, P<0.001, ANCOVA) even after controlling for BMI and weight. There was no significant difference between BN subjects with AN (n=10, 2.6±2.6 ng/ml) and those without AN (n=27, 3.8±2.4 ng/ml), despite lower BMI in BN with AN. Furthermore, leptin levels were decreased in BN without AN compared with healthy controls, even though BMI was comparable in these two subgroups. Plasma leptin concentrations were negatively correlated with baseline plasma cortisol levels (n=49, r=−0.49, P<0.001) and positively correlated with prolactin responses following l–tryptophan (n=49, r=0.37, P<0.009) and m–chlorophenylpiperazine (n=52, r=0.24, P<0.09). This is the first known report of decreased plasma leptin levels in BN. The decrement in leptin concentration is not related to BMI, body weight, or the presence or absence of BN. HPA axis activation as well as serotonin dysregulation may be related to decreased leptin levels, which may in turn contribute to disinhibited eating in BN. Although current leptin levels were not correlated with self-reported previous binge frequency, the role of leptin in the pathophysiology of BN deserves further study.
Leptin is a protein produced by the adipocyte–specific ob–ob gene which inhibits food intake ( Zhang et al., 1994, Halaas et al., 1995 and Campfield et al., 1995). Plasma levels have been reported to be altered in obesity ( Considine et al., 1996 and Kennedy et al., 1997) and anorexia nervosa (AN) ( Hebebrand et al., 1995, Heberand et al., 1997, Mantzoros et al., 1997, Grinspoon et al., 1996, Casanueva et al., 1997 and Ferron et al., 1997) but not in bulimia nervosa (BN) ( Ferron et al., 1997). We undertook the current study to precisely address the relationship between plasma leptin and body mass in BN in relationship to AN and other measures of pituitary/hypothalamic dysregulation. Given leptin's role in satiety in humans ( Heini et al., 1998), which is known to be altered in BN ( Brewerton, 1995), we also wondered if leptin was linked to other neurochemicals involved in eating, such as serotonin and cortisol. Mantzoros et al. (1997) reported significant relationships between levels of CSF leptin and CSF 5–hydroxyindole acetic acid (5–HIAA). We postulated that plasma leptin levels might also be correlated with other serotonergic measures, such as hormonal response to pharmacologic challenge agents, as well as to cortisol, which has been reported previously ( Licinio et al., 1997 and Korbonits et al., 1997).