Associations of gastric volumes, ingestive behavior, calorie and volume intake, and fullness in obesity

Buffet meal intake was inversely related to the ability to resist the urge to overeat. Factors associated with ingestive behavior significantly correlated with satiety and gastric accommodation. Gastric capacity during fasting is associated with calorie intake to the point of comfortable fullness; factors associated with ingestive behavior are associated with satiety and gastric accommodation.

Peripheral and central signals in the control of eating in normal, obese and binge-eating human subjects

The worldwide increase in the incidence of obesity is a consequence of a positive energy balance, with energy intake exceeding expenditure. The signalling systems that underlie appetite control are complex, and the present review highlights our current understanding of key components of these systems. The pattern of eating in obesity ranges from over-eating associated with binge-eating disorder to the absence of binge-eating. The present review also examines evidence of defects in signalling that differentiate these sub-types. The signalling network underlying hunger, satiety and metabolic status includes the hormonal signals leptin and insulin from energy stores, and cholecystokinin, glucagon-like peptide-1, ghrelin and peptide YY3-36 from the gastrointestinal tract, as well as neuronal influences via the vagus nerve from the digestive tract. This information is routed to specific nuclei of the hypothalamus and brain stem, such as the arcuate nucleus and the solitary tract nucleus respectively, which in turn activate distinct neuronal networks. Of the numerous neuropeptides in the brain, neuropeptide Y, agouti gene-related peptide and orexin stimulate appetite, while melanocortins and α-melanocortin-stimulating hormone are involved in satiety. Of the many gastrointestinal peptides, ghrelin is the only appetite-stimulating hormone, whereas cholecystokinin, glucagon-like peptide-1 and peptide YY3-36 promote satiety. Adipose tissue provides signals about energy storage levels to the brain through leptin, adiponectin and resistin. Binge-eating has been related to a dysfunction in the ghrelin signalling system. Moreover, changes in gastric capacity are observed, and as gastric capacity is increased, so satiety signals arising from gastric and post-gastric cues are reduced. Understanding the host of neuropeptides and peptide hormones through which hunger and satiety operate should lead to novel therapeutic approaches for obesity; potential therapeutic strategies are highlighted.

Physiological Effects of Bulimia Nervosa on the Gastrointestinal Tract

Bulimia nervosa is an eating disorder characterized by frequent bouts of binge eating accompanied by compensatory behaviour for preventing weight gain (purging). It is estimated that 3% to 5% of young women are affected by bulimia nervosa, and its prevalence is increasing. Bulimia nervosa afflicts both sexes and all races. It can lead to serious medical complications. The expression of the disease in the gastrointestinal tract may have a critical role in the diagnosis of bulimia nervosa. Physiological effects of bulimia nervosa on the gastrointestinal tract include dental caries and enamel erosion; enlargement of the parotid gland; esophagitis; changes in gastric capacity and gastric emptying; gastric necrosis; and alterations of the intestinal mucosa. Identification of any of these factors may aid in establishing an early diagnosis, which has been shown to increase the likelihood of recovery.