Reduced plasma level of diazepam-binding inhibitor (DBI) in patients with morbid obesity.

Peptides of the endozepine family, including diazepam-binding inhibitor (DBI), are regulatory neuropeptides originally isolated from rat brain tissue as factors potentially able to displace benzodiazepines from their binding sites [1]. DBI is widely expressed in the central nervous system, and high concentrations have been found in areas involved in the control of feeding behavior [1]. The biological effects of endozepines are mediated through three types of receptors: central-type benzodiazepine receptors (CBR), peripheral-type benzodiazepine receptors (PBR), and metabotropic receptors [1, 2]. It has been shown that injection of octadecaneuropeptide (ODN), which is a derivative of DBI, causes reduction in food consumption. Its anorexigenic effect is long-lasting, and leads to a substantial loss of weight [3]. Obesity is a worldwide epidemic leading to multiple complications. The term ‘morbid obesity’, or class III obesity according to the WHO, is used to describe adults with a body mass index (BMI) of 40 kg/m2 or more with significant medical problems caused by their weight. As there is currently lack of effective pharmacological therapy, efforts are underway to identify new factors which may be involved in its pathophysiology [4], and which possibly may be a target for future treatment or prevention. Pathophysiology of obesity is complex and not completely understood. Nevertheless, studies on the neuromodulatory changes in obese subjects [5–7], together with recent observations of endozepine pharmacology [1, 2], suggest that DBI, or one of its derivatives, may be a potential candidate for further research. This is the first pilot study to investigate, and confirm, the reduced plasma peripheral blood DBI concentration in patients with morbid obesity.