Gastric emptying and symptoms of bulimia nervosa: Effect of a prokinetic agent

Abstract

Objective Previous studies have suggested that delayed gastric emptying and abnormal postprandial release of hormones that influence satiation, particularly cholecystokinin (CCK), may play an important role in the pathophysiology of bulimia nervosa (BN). This study was designed to test these hypotheses as well as the efficacy of the prokinetic agent erythromycin in patients with BN. Method Thirty-two normal weight women with BN and 24 control participants consumed a large liquid test meal. Gastric emptying and pre- and postprandial release of CCK, peptide YY (PYY), and ghrelin were determined. Participants with BN were then recruited for double-blind treatment with erythromycin up to 500 mg three times daily vs. placebo for six weeks, following which they consumed a repeat test meal with gastric emptying and appetitive hormone measurements. Results CCK release at 15 minutes following the meal was marginally lower(p = 0.1) in BN than in control participants. Rate of gastric emptying and postprandial hormone release were similar in BN and controls. BN patients assigned to erythromycin compared to those assigned to placebo had more rapid gastric emptying following treatment, but there were no differences in release of CCK, PYY, or ghrelin following the post-treatment test meal. Moreover, treatment with erythromycin was not associated with clinical response. Discussion The current study does not support the clinical utility of moderate dose erythromycin in treating BN. Furthermore, the findings suggest that a modest increase in gastric emptying rate is associated neither with altered postprandial hormonal release nor with clinical benefit in these patients. While providing no evidence for the effectiveness of prokinetic agents in this setting, our findings do not preclude the possibility that a greater increase in gastric emptying rate might prove beneficial.

CCK response in bulimia nervosa and following remission

“…Consistent with a recent study [13] yet divergent from previous studies is the absence of a statistical difference in CCK response between the BN and CON groups. [3, 6].…”

“…Because CCK-8 is the predominant form used by investigators [10] and CCK- receptors in the alimentary pathway only bind to sulfated form [11], peripheral plasma concentrations of CCK-8S were measured using a radioimmunoassay (RIA) that also detects the bioactive forms of CCK-58, CCK-33, and CCK-22 [12]. This is consistent with previous studies of CCK and satiety and will allow, in this patient population, for comparison across studies [13]…”

“…When examining the 15-minute mean peak response, as done in a previous report [13], there was no significant difference between the BN (2.33 ± 2.69 pmol/L), RBN (2.59 ± (2.67), or CON (4.23 ± 2.91), ( p = 0.1), groups respectively.…”

“…ghrelin) peptides [25, 26] and eating related pathways [27]. Emphasis should be focused on research that explores pharmacotherapeutic agents that may have an effect on increasing CCK levels [13]. It would be informative to evaluate if increased CCK levels would decrease binge/vomit behaviors and or increase urge to vomit in those with BN.…”

Reduction in total plasma ghrelin levels following catecholamine depletion: Relation to bulimic and depressive symptoms

“…In line with the increased food intake in BN, patients with the disorder have been reported to have elevated ghrelin concentrations at baseline (Kojima et al, 2005;Prince et al, 2009;Tanaka et al, 2002Tanaka et al, , 2003. However, some studies are in disagreement with these findings, showing normal (Devlin et al, 2012;Monteleone et al, 2005Monteleone et al, , 2008Troisi et al, 2005) or decreased (Monteleone et al, 2003) ghrelin levels in BN.…”