Association of Nesfatin-1, Acylated Ghrelin and Cortisol with Scores of Compulsion, Food Addiction, and Binge Eating in Adults with Normal Weight and with Obesity

Abstract

Background/Aims: The alterations of eating behavior are insufficiently recognized in the clinical attention of adults with obesity. The objective of this study was to examine the characteristics of overeating behavior and its association with depression, perceived stress, acylated ghrelin, nestafin-1, and cortisol. Methods: This cross-sectional comparative study included 80 participants with obesity and 50 with normal weight. The volunteers completed questionnaires to evaluate symptoms of food addiction (FA), obsessive compulsive, binge eating (BE), depression, and perceived stress. We measured glucose, lipids, acylated ghrelin, nesfatin-1, and insulin in a fasting blood sample as well as urine cortisol. We compared groups with students t test, and analysis of variance, and tested associations by logistic and multiple regression. Results: By multiple regression, the BE total score was positively associated with the FA (p < 0.0001) and depression total score (p < 0.0001). By logistic regression, the positive score of FA was associated with ghrelin (p < 0.02). The perceived stress total score was associated negatively with cortisol (p < 0.0006). Conclusion: The BE and FA are strongly associated in agreement with the concept that both conditions have overlapping features. Depressive symptoms are associated with symptoms of disordered eating ­behavior. FA positive score was associated with ghrelin. BE total score was associated with nesfatin-1.

Analysis of genome-wide DNA methylation patterns in obesity

“…Calcium ions can inhibit the progression of obesity by promoting adipocyte differentiation and metabolism to increase energy consumption [40,41]. Leptin, neuropeptide Y, Nxafatine-1 and other signaling molecules can regulate the feeding center and peripheral satiety system through calcium signaling pathways to reduce food intake and energy acquisition, thereby reducing obesity [42,43]. Our results show that these differentially methylated genes may play important roles in the development of obesity by regulating key biological processes and pathways.…”

Calcium Signaling Pathways: Key Pathways in the Regulation of Obesity

“…Some researchers have shown that the animal feeding process is inseparable from the regulation of the central feeding system and the peripheral satiety system [39]. The results of many studies have suggested that a variety of signaling molecules are involved in feeding regulation, including CCK (cholecystokinin), LP (leptin), NPY (neuropeptide Y), and Nesfatin-1 [8,9]. In this part, we mainly summarize the regulation of Nesfatin-1, which may decrease the occurrence of obesity through calcium signaling pathways.…”

“…They found that calcium ions could be important in enhancing the energy consumption by promoting adipocytes differentiation and metabolism, thereby reducing obesity [4,5,6,7]. In addition to promoting energy consumption, signal molecules such as Leptin, Neuropeptide Y, and Nesfatin-1 could regulate the feeding center and the peripheral satiety system through calcium signaling to decrease food intake and reduce the energy acquisition, thereby decreasing obesity [8,9]. Here, we review the effects of the biological clock, the intestinal microbial activity, and the nerve excitability on the regulation of the incidence of obesity, highlighting the role of multiple calcium signaling pathways in these regulation processes.…”

Combined Effects of High-Intensity Aerobic Exercise Training and Ziziphus jujuba Extract on Tissue Nesfatin-1 in Rats

“…showed that nesfatin-1 concentration increased after insulin, dexamethasone, (100nM), IL-6 (20ng/mL) administration, and decreased after TNF-α administration (10ng/mL) ( 14 ). In addition, they reported that the concentration of nesfatin-1 has a negative correlation with cortisol ( 34 ). Thus, it seems that besides energy source, any change in inflammatory markers might have an impact on tissue and plasma nesfatin-1 concentrations.…”