Role of Glucagon-Like Peptide-1 in Appetite Regulation in Patients with Morbid Obesity and Leptin Resistance

To contribute to the outstanding discussion of suggested reasons of obesity, including the hormonal disorders, and how to deal and avoid them, this research attempts to investigate and control the energy balance disturbances resulting from hormonal disorders that may cause obesity by dysregulating appetite. A total of 88 participants are recruited, among whom 50 and 38 were allocated to the control and patients groups, respectively. Venous blood samples are collected from the participants at different time points for the quantification of the pre-prandial and 2, 6 and 12 h postprandial levels of lipid markers, including total cholesterol, high density lipoproteins, low density lipoproteins, very low density lipoproteins, and triacylglycerol, and the appetite-related hormones leptin and intestinal hormones glucagon-like peptide (GLP-1). In healthy controls, leptin levels increased prior to eating, decreased after eating, and then increased to induce hunger at several hours after eating. By contrast, the pre-prandial and postprandial leptin levels of the patients group did not show statistically significant differences. Healthy controls had moderate GLP-1 levels, whereas patients with obesity and leptin resistance had high GLP-1 levels. The GLP-1 was found to be secreted in response to high postprandial energy levels as an adaptation to leptin resistance. This study elucidates the relationship between the adipose tissue hormone leptin and GLP-1 in patients with morbid obesity. Findings of using GLP-1 as an appetite regulator for the morbidly obese patients and have leptin resistance (resistance to its action in appetite regulation), presented here, should provide a valuable information for further experimental investigations.