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Food intake regulation is generally evaluated by many aspects consisting of complex mechanisms, including homeostatic regulatory mechanism, which is based on negative feedback, and hedonic regulatory mechanism, which is driven by a reward system. One important aspect of food intake regulation is the peripheral hormones that are secreted from the gastrointestinal tract. These hormones are secreted from enteroendocrine cells as feedback to nutrient and energy intake, and will communicate with the brain directly or via the vagus nerve. Gastrointestinal hormones are very crucial in maintaining a steady body weight, despite variations in nutrient intake and energy expenditure. In this review, we provide an overview of the regulation of feeding behavior by gut hormones, and its role in obesity treatments.

Obesity has a prevalence of 15-30% among European and American populations. It is an incurable chronic disease associated with considerable mortality and co-morbidity. The co-morbidity risk can be reduced substantially by a moderate weight loss of 5-15%. Notably, additional weight gain exacerbates the morbidity of any concurrent disease. Obesity is also recognized as the basis for metabolic syndrome. Recent research has shown that adipocytes secrete various hormones and cytokines that contribute to obesity. Leptin is an adipostatic hormone that acts on receptors in the hypothalamus to suppress food intake and increase energy consumption. Reduced sensitivity to this molecule can trigger the onset of obesity. Neuropeptides such as leptin also affect salivary secretion. Various neuropeptides have been identified in saliva; the associated receptors are located in the salivary glands or in the nerves innervating the salivary glands. Obesity is associated with hyposalivation and thereby related to several aspects of oral health, such as caries and periodontitis. Hyposalivation is a severe morbidity that can lead to a precipitous decline in oral hygiene, which further leads to multifocal dental caries and periodontitis, or even cardiac disorders. In this article, we review the relationship between salivary secretion and neuropeptides known to play a role in obesity., (© 2013 Asian Oceanian Association for the Study of Obesity. Published by Elsevier Ltd. All rights reserved.)

Objective: The aim of this study was to examine the associations of klotho with body mass index (BMI) in patients with restricting-type anorexia nervosa (r-AN) and obesity., Method: We examined plasma klotho as well as adiponectin and its isoform levels in comparison in 11 obese patients, 12 r-AN patients, and 11 control participants., Results: Plasma klotho levels were markedly lower in the obesity and r-AN groups than in the control group. Moreover, plasma klotho levels increased significantly after the recovery of BMI in r-AN patients. Total and high-molecular-weight adiponectin levels were significantly decreased only in obesity. There was no relationship between klotho and total adiponectin levels or klotho and respective adiponectin isoform levels in the entire study population., Conclusions: These results suggest that klotho may reflect normal nutritional state, and that the decrease of klotho in r-AN and obesity may underlie the deteriorating processes of these disorders., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Obese individuals often have increased appetite despite normal plasma levels of the main orexigenic hormone ghrelin. Here we show that ghrelin degradation in the plasma is inhibited by ghrelin-reactive IgG immunoglobulins, which display increased binding affinity to ghrelin in obese patients and mice. Co-administration of ghrelin together with IgG from obese individuals, but not with IgG from anorectic or control patients, increases food intake in rats. Similarly, chronic injections of ghrelin together with IgG from ob/ob mice increase food intake, meal frequency and total lean body mass of mice. These data reveal that in both obese humans and mice, IgG with increased affinity for ghrelin enhances ghrelin's orexigenic effect, which may contribute to increased appetite and overeating.

Background: Obestatin is a recently identified ghrelin gene product that was reported to inhibit appetite and gastric motility in contrast to ghrelin. We investigated fasting obestatin and ghrelin levels in patients with obesity and anorexia nervosa., Methods: Fasting plasma obestatin, acyl-ghrelin, desacyl-ghrelin, leptin, glucose serum adiponectin, and insulin were measured in 10 obese subjects, 11 restricting-type anorexics, and 11 control subjects., Results: Obese group had significantly lower levels of obestatin (p < .01), while anorexic group had significantly higher levels (p < .01). Obestatin was negatively correlated with body mass index (BMI) (r = -.74), glucose (r = -.56), insulin (r = -.55), leptin (r = -.66), and also with the homeostasis model assessment of insulin resistance (HOMA-R) (r = -.49) and was positively correlated with acyl-ghrelin (r = .65) and desacyl-ghrelin (r = .60). No correlation was seen between obestatin and adiponectin, but the latter was negatively correlated with both acyl-ghrelin and desacyl-ghrelin. Desacyl-ghrelin to acyl-ghrelin ratio was significantly different between anorexic and control groups (p < .05), while no difference was seen between obese and control groups., Conclusions: Both obestatin and ghrelin are increased in anorexic and decreased in obesity. We suggest that obestatin is a nutritional marker reflecting body adiposity and insulin resistance.