Objectives: Craniopharyngiomas are rare low-grade tumors located in the hypothalamic and/or pituitary region. Hypothalamic involvement and treatment resulting in hypothalamic damage are known to lead to development of "hypothalamic obesity" (HyOb) in 50% of cases. The management of HyOb, associated with eating disorders and rapid comorbidities, is an important issue. Bariatric surgery is the most effective therapy for weight loss in patients with severe exogenous obesity. The aim of this systematic review and meta-analysis was to determine the 12-month outcome of bariatric surgery for HyOb due to craniopharyngioma treatment. Methods and Results:Relevant studies were identified by searches of the MEDLINE and EMBASE databases until January 2013. A total of 21 cases were included: 6 with adjustable gastric banding, 8 with sleeve gastrectomy, 6 with Roux-en-Y gastric bypass, and 1 with biliopancreatic diversion. After data pooling, mean weight difference was Ϫ20.9 kg after 6 months (95% confidence interval [CI], Ϫ35.4, Ϫ6.3) and Ϫ15.1 kg after 12 months (95% CI, Ϫ31.7, ϩ1.4). The maximal mean weight loss was achieved by the gastric bypass group: Ϫ31.0 kg (95% CI, Ϫ77.5, ϩ15.5) and Ϫ33.7 kg (95% CI, Ϫ80.7, ϩ13.3) after 6 and 12 months, respectively. Conclusions:In this largest ever published study on the effect of bariatric surgery on obesity after craniopharyngioma treatment, we observed an important weight loss after 1 year of follow-up. Larger studies are warranted to establish appropriate selection criteria and the best surgical technique to perform bariatric surgery. (J Clin Endocrinol Metab 98: 2239 -2246, 2013) C raniopharyngiomas are benign, slow-growing tumors that are located within the sellar and parasellar region of the central nervous system. There are 2 histological types: the adamantinomatous tumors, mostly seen in children, which arise from epithelial remnants of the Rathke's pouch; and the squamous papillary form, seen in adults. The incidence rate ranges from 0.5 to 2 per million subjects/year, with a peak between 5 and 14 years of age, although craniopharyngiomas can occur at any age (1).Tumor resection, with or without radiotherapy, represents the therapeutic standard of care. After treatment, obesity and eating disorders are observed in 40 -50% of patients (2-4). Weight gain is also observed at diagnosis before treatment in some patients. Risk factors for the development of obesity after treatment of craniopharyngioma include younger age at diagnosis, presence of endocrinopathy whatever type, initial symptoms of intracranial hypertension, greater body mass index (BMI) at diagnosis, familial predisposition for obesity, and hypothalamic involvement. In addition, pterional surgery, multiple surgery, and hypothalamic irradiation with doses greater than 51 Gy have been associated with the development of obesity (3,(5)(6)(7).The cause of weight gain in this setting is incompletely understood, but it is believed to be due to "endogenous" mechanisms, rather than the more common form of "exogenous" obesit...

Melanocortin-4 receptor (MC4R) mutations are the most common known cause of monogenic obesity and an important contributor to polygenic obesity. MC4R mutations with partial or total loss of function, as well as the variant rs17782313 mapped near MC4R, are positively associated with obesity. MC4R is involved in the leptin-melanocortin signalling system, located in hypothalamic nuclei, that controls food intake via both anorexigenic or orexigenic signals. Impairment in this receptor might affect eating behaviours. Thus, in the case of MC4R mutation carriers, obesity could be related, at least partly, to inadequate control over eating behaviours. Many published studies address eating behaviours in MC4R mutation carriers. Most studies focus on binge eating disorder, whereas others examine various aspects of intake and motivation. Up to now, no evaluation of this literature has been performed. In this review, we examine the available literature on eating behaviours in carriers of MC4R mutations and variant rs17782313 near MC4R gene. We address binge eating disorder, bulimia nervosa, mealtime hyperphagia, snacking, psychological factors, satiety responsiveness and intake of energy and macro/micronutrient. In a small number of studies, MC4R mutations seem to impair eating behaviours or motivation, but no clear causal effects can be found in the balance of the evidence presented. Improvements in methodologies will be necessary to clarify the behavioural effects of MC4R mutations.