The Role of BDNF, Leptin, and Catecholamines in Reward Learning in Bulimia Nervosa

Abstract

Background:A relationship between bulimia nervosa and reward-related behavior is supported by several lines of evidence. The dopaminergic dysfunctions in the processing of reward-related stimuli have been shown to be modulated by the neurotrophin brain derived neurotrophic factor (BDNF) and the hormone leptin.Methods:Using a randomized, double-blind, placebo-controlled, crossover design, a reward learning task was applied to study the behavior of 20 female subjects with remitted bulimia nervosa and 27 female healthy controls under placebo and catecholamine depletion with alpha-methyl-para-tyrosine (AMPT). The plasma levels of BDNF and leptin were measured twice during the placebo and the AMPT condition, immediately before and 1 hour after a standardized breakfast.Results:AMPT–induced differences in plasma BDNF levels were positively correlated with the AMPT–induced differences in reward learning in the whole sample (P=.05). Across conditions, plasma brain derived neurotrophic factor levels were higher in remitted bulimia nervosa subjects compared with controls (diagnosis effect; P=.001). Plasma BDNF and leptin levels were higher in the morning before compared with after a standardized breakfast across groups and conditions (time effect; P<.0001). The plasma leptin levels were higher under catecholamine depletion compared with placebo in the whole sample (treatment effect; P=.0004).Conclusions:This study reports on preliminary findings that suggest a catecholamine-dependent association of plasma BDNF and reward learning in subjects with remitted bulimia nervosa and controls. A role of leptin in reward learning is not supported by this study. However, leptin levels were sensitive to a depletion of catecholamine stores in both remitted bulimia nervosa and controls.

Is Serum BDNF Altered in Acute, Short- and Long-Term Recovered Restrictive Type Anorexia Nervosa?

“…One comprehensive study on serum BDNF concentrations in a sample comprised of individuals with AN, BN and binge-eating disorder (BED) reported decreased BDNF levels in AN and BN, but not in BED [ 17 ]. Peripheral BDNF concentrations appear to be generally lower in BN [ 81 ] and may recover with therapy [ 82 ], but one study found a significant relationship with reward-related learning in a sample of remitted patients [ 83 ]. Studies on BDNF in other psychiatric conditions including major depressive disorder [ 14 , 84 ] and anxiety in general, and obsessive-compulsive disorder in particular [ 16 ], have similarly reported decreased BDNF levels.…”

Brain-Derived Neurotrophic Factor, Depression, and Physical Activity: Making the Neuroplastic Connection

“…Berton and colleagues demonstrated that chronic stress increased BDNF levels within the nucleus accumbens [ 141 ], whereas virally mediated knockdown of BDNF in this region reduced social aversion following chronic social defeat [ 141 ], suggesting that increased BDNF in the ventral tegmental area and nucleus accumbens is positively associated with plasticity-induced aversive learning [ 142 – 144 ]. Finally, rodents with a knockdown of the BDNF gene in the ventral tegmental area consumed greater amounts of high-fat diet foods [ 145 ], whereas Goto-Kakizaki rats administered intracerebroventricular injections of BDNF exhibited suppressed feeding [ 146 ], a finding that underscores the modulating effects of BDNF on feeding behaviors and its interactions with the mesolimbic dopaminergic reward system [ 147 ].…”

KoreanCurcuma longa L. induces lipolysis and regulates leptin in adipocyte cells and rats

“…Leptin, the product of the obesity gene, is an important hormone involved with feeding behavior, and its concentration in blood is increased in direct proportion to the amount of body fat [ 4 ]. When leptin is carried to the brain through the circulatory system, it is combined with leptin receptors of hypothalamic nerve cells that feeds the regulatory center and sends signals to the brain.…”

“…When leptin is carried to the brain through the circulatory system, it is combined with leptin receptors of hypothalamic nerve cells that feeds the regulatory center and sends signals to the brain. This affects energy consumption, the metabolism of carbohydrate and fat, and body weight control [ 4 ]. Active research is examining the association of leptin and feeding behavior, hypothesizing that body weight control is related to obesity, and leptin is being used as the standard evaluating obesity [ 5 ].…”