Salivary concentrations of cytokines and other analytes in healthy children.

BACKGROUND: Blood has been the usual biological fluid for measuring analytes, but there is mounting evidence that saliva may be also useful for detecting cytokines in a noninvasive way. Thus, in this study we aimed to determine concentration of cytokines and other analytes in saliva from a population of healthy children. METHODS: We collected un-stimulated whole saliva samples from clinically healthy children, and concentration of 17 cytokines and 12 other analytes were measured in supernatants. All values were adjusted by albumin content and were log-transformed before multivariate statistical analysis. RESULTS: We included 114 children (53.5% females) between 6.0 and 11.9 years old. The highest concentrations (medians, pg/µg albumin) were seen for visfatin (183.70) and adiponectin (162.26) and the lowest for IL-13 and IL-2 (~0.003). Albumin concentration was associated with age (rS = 0.39, p < 0.001). In the multivariate analysis, five analytes (C peptide, ghrelin, GLP-1, glucagon, leptin) inversely correlated with age and positively with height-for-age. Age was also positively associated with PAI-1, while height-for-age was also positively associated with insulin and visfatin. Finally, BMI-for-age had a positive correlation with GM-CSF and insulin. CONCLUSIONS: Herein, we provided concentration values for 29 analytes in saliva from healthy children that may be useful as preliminary reference framework in the clinical research setting.

Is Ghrelin Synthesized in the Central Nervous System?

Ghrelin is an octanoylated peptide that acts via its specific receptor, the growth hormone secretagogue receptor type 1a (GHSR-1a), and regulates a vast variety of physiological functions. It is well established that ghrelin is predominantly synthesized by a distinct population of endocrine cells located within the gastric oxyntic mucosa. In addition, some studies have reported that ghrelin could also be synthesized in some brain regions, such as the hypothalamus. However, evidences of neuronal production of ghrelin have been inconsistent and, as a consequence, it is still as a matter of debate if ghrelin can be centrally produced. Here, we provide a comprehensive review and discussion of the data supporting, or not, the notion that the mammalian central nervous system can synthetize ghrelin. We conclude that no irrefutable and reproducible evidence exists supporting the notion that ghrelin is synthetized, at physiologically relevant levels, in the central nervous system of adult mammals.

Evaluation of immunohistochemical expression of ghrelin-producing rectal cells in Wistar rats underwent to the cafeteria diet

PURPOSE:To investigate the impact of cafeteria diet on ghrelin expression in rectal tissue and identify the morphologic cell type. METHODS:Twenty-four male Wistar rats were divided into four subgroups of six animals each: RC1 (rat chow 1) and CAF1 (cafeteria diet 1) for a period of 30 days; RC2 (rat chow 2) and CAF2 (cafeteria diet 2) for a period of 60 days. The animal and rectal weight, the number and the type of immunoreactive ghrelin cells were recorded and compared between the subgroups. The statistical study was established by ANOVA and Student's t test. RESULTS:There was no difference in the total of immunoreactive cells (p=0.685) between the subgroups nor between weight and presence or absence of ghrelin expression (p=0.993). All the immunoreactive cells identified were closed-type. CONCLUSION:The cafeteria diet did not have influence on the amount of immunoreactive rectal cells of ghrelin and only one type (closed-type) of immunoreactive cells was expressed in the rectum.

Evaluation of immunohistochemical expression of ghrelin-producing rectal cells in Wistar rats receiving the cafeteria diet.

PURPOSE: To investigate the impact of cafeteria diet on ghrelin expression in rectal tissue and identify the morphologic cell type. METHODS: Twenty-four male Wistar rats were divided into four subgroups of six animals each: RC1 (rat chow 1) and CAF1 (cafeteria diet 1) for a period of 30 days; RC2 (rat chow 2) and CAF2 (cafeteria diet 2) for a period of 60 days. The animal and rectal weight, the number and the type of immunoreactive ghrelin cells were recorded and compared between the subgroups. The statistical study was established by ANOVA and Student's t test. RESULTS: There was no difference in the total of immunoreactive cells (p=0.685) between the subgroups nor between weight and presence or absence of ghrelin expression (p=0.993). All the immunoreactive cells identified were closed-type. CONCLUSION: The cafeteria diet did not have influence on the amount of immunoreactive rectal cells of ghrelin and only one type (closed-type) of immunoreactive cells was expressed in the rectum.

Density of ghrelin-producing cells is higher in the gastric mucosa of morbidly obese patients.

BACKGROUND: Ghrelin is a peptide mainly secreted by gastric mucosa and has been implicated in the regulation of eating behavior and weight balance. Obesity and Helicobacter pylori infection are associated with changes in plasma ghrelin levels. OBJECTIVE: This study was designed to evaluate the density of ghrelin-producing cells in the gastric mucosa of morbidly obese and dyspeptic non-obese patients, with and without H. pylori infection. METHODS: Gastric biopsies of the antral and oxyntic mucosa were obtained from 50 morbidly obese patients (BMI >40, 21 with metabolic syndrome (MS)), 17 dyspeptic overweight subjects (25

Biliopancreatic diversion induces villi elongation and cholecystokinin and ghrelin increase.

INTRODUCTION: Factors leading to weight loss and weight stabilization after bariatric surgery are not fully understood. Our aim was to evaluate, in Sprague-Dawley rats, the histological and gut hormonal changes after Larrad-biliopancreatic diversion (Larrad-BPD). MATERIALS AND METHODS: Rats randomly underwent the following protocols: Larrad-BPD (n=4) versus pair fed (PF) (n=4). Weight and food intake were measured every day. By immunohistochemistry ghrelin was examined in the stomach, while cholecystokinin (CCK), glucagon-like-peptide-1 (GLP-1), peptide YY (PYY) and serotonin (5-HT) expression were analyzed in alimentary limb and ileum following or not the Larrad-BPD. RESULTS: Larrad-BPD rats exhibited significant (P<0.05) weight loss compared to PF rats. Villi enlongation was observed in Larrad-BPD rats. In residual stomach, ghrelin was diminished. In the alimentary limb, ghrelin and CCK positive cells were detected more than in the ileum of PF rats. GLP-1 expression was decreased and PYY expression was absent after Larrad-BPD compared with PF rats. DISCUSSION: Larrad-BPD is followed by histological changes and a pleiotropic gut endocrine response aimed to compensate the reduction of intestinal area exposed to food. Until now, the hormones responsible for the intestinal hypertrophy have not been defined.

Effect of Helicobacter pylori infection on gastric ghrelin expression and body weight.

BACKGROUND & AIM: Ghrelin is a peptide mainly produced by gastric tissue playing an important role in energy homeostasis. It has been suggested that inflammatory and atrophic events induced by Helicobacter pylori (H. pylori) infection in gastric mucosa compromise the survival of the ghrelin-producing cells. The aim of this study was to investigate the effect of H. pylori infection on gastric ghrelin expression and body weight. METHODS: Consecutive patients referred for upper endoscopy were invited to participate. Patients with H. pylori infection (determined by histology) were defined as cases and patients without infection as controls. The density of colonization was classified in mild, moderate, or severe infection. Body mass index (BMI) was calculated. Ghrelin-immunoreactive cells were quantified in gastric biopsies by immunohistochemical staining. RESULTS: We studied 189 cases (92 males, 97 females) and 94 controls (55 males, 39 females). Cases were older (48.16 +/- 16.44 vs. 42.88 +/- 17.04 years, p < 0.05) and exhibited a lower percentage of ghrelin-immunoreactive cells (2.13% vs. 10.43%, p < 0.05) than controls. The prevalence of obesity was significantly lower than normal-weight among all cases, independently of the severity of infection (mild infection, 17.6% vs. 47.3%, p = 0.001; moderate-severe infection, 10.4% vs. 50%, p = 0.001). Univariate analysis showed a non-significant trend suggesting a protective effect of H. pylori against obesity. Nevertheless, BMI did not differ significantly between cases and controls. CONCLUSION: Chronic H. pylori infection contributes to a lower percentage of gastric ghrelin-immunoreactive cells but has no effect on the body weight of infected patients.