Fasting and postprandial levels of ghrelin, leptin and insulin in lean, obese and anorexic subjects

Abstract

IntroductionGhrelin, leptin and insulin are involved in neurohormonal regulation of energetic homeostasis.AimWe investigated the correlation between nutritional status and plasma levels of leptin, ghrelin and insulin in lean, obese and anorexic subjects.Material and methodsNineteen obese and 18 anorexic adults were enrolled in the study. Seventeen adults with normal body mass index (BMI) served as controls. Blood samples were taken twice: before breakfast and 2 h after breakfast. Fasting and postprandial ghrelin, leptin and insulin were examined. The following correlations were estimated: between BMI and basal level of tested hormones, between insulin and ghrelin, and between insulin and leptin. The threshold level of significance was p ≤ 0.05 for all calculations.ResultsBasal insulin level was lowest in anorexic patients and greatest in obese subjects. Fasting plasma ghrelin was lower in obesity and higher in anorexia as compared with the controls. Comparing with controls, fasting leptin levels were higher in obese and lower in anorexic subjects. There was positive correlation between BMI and basal leptin level in obesity. A significant postprandial increase was noted for insulin in all studied groups. Increased leptin and decreased ghrelin levels were detected 2 h after a meal in the control group. In obese patients, postprandial leptin was lower than before food intake, and fasting leptin showed positive correlation with basal insulin level.ConclusionsBasal plasma ghrelin, leptin and insulin levels differ according to nutritional status. Impaired ghrelin and leptin secretion and insulin sensitivity may be involved in the pathogenesis of eating disorders.

Postprandial leptin and adiponectin in response to sugar and fat in obese and normal weight individuals

“…For normal weight individuals, one study showed that leptin decreased at 6 h [44] such as in our study, unchanged in other studies [18,19], whereas an increase was observed in other reports [20][21][22]. In obese individuals two reports showed a significant postprandial decrease in leptin [21,22], as well as no postprandial leptin changes were observed in other studies [18,19]. Finally, opposite to our observation of the secretion of adiponectin, no initial close to significant, increase of leptin was observed.…”

“…These results contradict for the most other reports. For normal weight individuals, one study showed that leptin decreased at 6 h [44] such as in our study, unchanged in other studies [18,19], whereas an increase was observed in other reports [20][21][22]. In obese individuals two reports showed a significant postprandial decrease in leptin [21,22], as well as no postprandial leptin changes were observed in other studies [18,19].…”

“…Furthermore, our knowledge of postprandial changes of leptin and adiponectin in normal weight and obese individuals is limited. The results are diverging, both for postprandial leptin and adiponectin secretion, with reports of no postprandial changes in leptin [18][19][20], as well as increased postprandial leptin levels in normal weight controls and decreased in obese individuals [21,22]. For adiponectin, reports have found both increased [23][24][25] and unchanged [25][26][27][28][29] for both normal weight and obese individuals.…”

Mexico City normal weight children exposed to high concentrations of ambient PM2.5 show high blood leptin and endothelin-1, vitamin D deficiency, and food reward hormone dysregulation versus low pollution controls. Relevance for obesity and Alzheimer disease

“…Thus, high leptin and low ghrelin suppress the appetite, while low GLP-1 and glucagon contribute to appetite stimulation. The final effect on a child will also depend on meal content, the amount of high-fat and sugar, including fructose, the amount and distribution of body and liver fat content, the effects on insulin sensitivity and glucose metabolism, the basal nutritional status, gonadal status, exercise level, the integrity of the brain-gut axis, and their genetic susceptibility for diabetes mellitus (Bouret, 2013;Pettus et al, 2013;Korek et al, 2013;Shah and Vella, 2014;Liu et al, 2014aLiu et al, , 2014bLiu et al, , 2014cLaughlin,2014). Low levels of ghrelin are of concern in children given its involvement in the regulation of growth hormone, memory and learning, food addiction and neuroprotection (Albarran-Zeckler et al, 2011).…”

Ghrelin and Obesity: Identifying Gaps and Dispelling Myths. A Reappraisal

“…Insight into the modification of the endogenous ghrelin system seems to be promising not only for the control of obesity, but also for the management of clinically significant anorexia and pathological weight reduction. Accumulating evidence has shown that in patients with anorexia nervosa, there is a paradoxical increase in plasma ghrelin level even when compared with matched controls or obese patients (26), suggesting that there might be an insensitivity to ghrelin (27). Moreover, in vitro studies have documented that intra-peritoneal or systemic administration of ghrelin has the potential to improve the appetite and the nutritional status, and at the same time reduce the metabolic rate in patients with end-stage cancer (5).…”