Prader-Willi syndrome (PWS) is a contiguous gene syndrome characterized by uncontrollable eating or hyperphagia. Several studies have confirmed that plasma ghrelin levels are markedly elevated in PWS adults and children. The study of anorexigenic hormones is of interest because of their regulation of appetite by negative signals. To study the pattern and response of the anorexigenic hormones such as cholecystokinin (CCK) and peptide YY (PYY) to a meal in PWS, we measured the plasma CCK, PYY, ghrelin and serum insulin levels in PWS patients (n=4) and in controls (n=4) hourly for a day, and analyzed hormone levels and hormonal responses to meals. Repeated measures of ANOVA of hormone levels demonstrated that only insulin levels decreased (p=0.013) and CCK (p=0.005) and ghrelin (p=0.0007) increased in PWS over 24 hr. However, no significant group x time interactions (ghrelin: p=0.89, CCK: p=0.93, PYY: p=0.68 and insulin: p=0.85) were observed; in addition, there were no differences in an assessment of a three-hour area under the curve after breakfast. These results suggest that the response pattern of hormones to meals in PWS patients parallels that of normal controls. In addition, the decrease of insulin levels over 24 hr, in spite of obesity and elevated ghrelin levels, suggests that the baseline insulin level, not the insulin response to meals, may be abnormal in patients with PWS.
Adolescent ; Area Under Curve ; Biopsy ; Body Mass Index ; Body Weight ; Child ; Cholecystokinin/*blood ; Ghrelin ; Humans ; Insulin/*blood/metabolism ; Male ; Obesity ; Peptide Hormones/*blood/metabolism ; Peptide YY/*blood ; Prader-Willi Syndrome/*blood ; Time Factors

OBJECTIVETo study the effect of Jiaweisinisan (JWSNS), a traditional Chinese herbal medicinal recipe, on gastric mucosal ultrastructure and brain-gut axis in rat models of chronic psychological stress and elucidate the mechanism of JWSNS for ameliorating stress-induced gastrointestinal dysfunction.

METHODSSixty rats were randomly assigned into normal control group, model group, 3 JWSNS groups (high, moderate, and small doses), and omeprazole group (n=10). Rat models of chronic psychological stress were established by random stressful stimulations, and following the corresponding interventions, plasma adrenocorticotropic hormone (ACTH) and cortisol (CORT) levels were detected using radioimmunoassay, and the mRNA expressions of gastrin receptor in the gastric tissue (GASR) and vasoactive intestinal peptide II receptor (VIPR2) in the jejunal tissue were examined using RT-PCR. Transmission electron microscopy was employed to examine the ultrastructural changes in the gastric mucosa tissue cells of the glandular stomach area and alterations in the intercellular junctions.

RESULTSElectron microscopy revealed obvious damages in gastric mucosal epithelial cell organelles and nuclei in the model rats. These damages were ameliorated after treatments with JWSNS and omeprazole. Compared with the model group, the 3 JWSNS groups and omeprazole group all showed significantly lowered plasma ACTH and CORT levels, increased gastrin receptor mRNA expression and decreased jejunal VIPR2 mRNA expression (P<0.05 or 0.01).

CONCLUSIONJWSNS can obviously ameliorate the pathologies of the gastric mucosa cells, regulate the state of brain-gut axis, and modulate the gastric gastrin receptor and jejunal VIPR2 mRNA expressions in rats with chronic psychological stress.

Adrenal Cortex Hormones ; blood ; Adrenocorticotropic Hormone ; blood ; Animals ; Drugs, Chinese Herbal ; pharmacology ; Gastric Mucosa ; metabolism ; pathology ; ultrastructure ; Hydrocortisone ; blood ; Jejunum ; metabolism ; Male ; Rats ; Rats, Wistar ; Receptors, Bombesin ; metabolism ; Receptors, Vasoactive Intestinal Peptide, Type II ; metabolism ; Stress, Psychological ; pathology

OBJECTIVETo investigate the effects of long-term high-protein, low-carbohydrate diet on body weight and the expression of gastrointestinal hormones in diet-induced obesity rats.

METHODSTwenty-four diet-induced obesity rat models were established by feeding fat-enriched diet, then were randomly divided into two groups by stratified sampling method by weight: the high-protein diet group (HP, 36.7% of energy from protein), and the normal chow group (NC, 22.4% of energy from protein), 12 rats in each group. The total calorie intake of each rat per day was similar and was maintained for 24 weeks, then body weight, visceral fat mass, fasting plasma ghrelin and glucagon-like peptide-1 (GLP-1) were determined, as well as protein expression of ghrelin in stomach, GLP-1 in ileum were detected by immunohistochemistry.

RESULTSAfter 24 weeks, body weight of HP, NC groups were (490.92 ± 39.47) g and (545.55 ± 31.08) g, respectively (t = -3.664, P < 0.01); visceral fat mass were (22.42 ± 7.04) g and (32.33 ± 9.27) g, respectively (t = -2.503, P < 0.05); plasma ghrelin level were (2.36 ± 0.82) and (1.95 ± 0.64) ng/ml, respectively (t = 1.337, P > 0.05), and plasma ghrelin level was negatively correlated to body weight (r = -0.370, t = -1.899, P < 0.05), visceral fat mass (r = -0.454, t = -2.52, P < 0.01); plasma GLP-1 concentration were (0.52 ± 0.13) and (0.71 ± 0.19) ng/ml, respectively(t = -2.758, P < 0.05); ghrelin protein expression in stomach were 25 473 ± 8701 and 10 526 ± 6194, respectively (t = 2.501, P < 0.05); GLP-1 protein expression in ileum were 27 431 ± 5813 and 36 601 ± 5083, respectively (t = -1.833, P = 0.081).

CONCLUSIONLong-term isocaloric high-protein, low-carbohydrate diet can reduce body weight and visceral fat, increase the expression of ghrelin, and decline GLP-1 expression in diet-induced obesity rats.

Animals ; Body Weight ; Diet, Carbohydrate-Restricted ; Dietary Proteins ; administration & dosage ; Gastrointestinal Hormones ; metabolism ; Ghrelin ; blood ; metabolism ; Glucagon-Like Peptide 1 ; metabolism ; Intra-Abdominal Fat ; metabolism ; Male ; Obesity ; metabolism ; Rats ; Rats, Wistar

Recently, gastric Helicobacter pylori (H. pylori) colonization has been shown to affect the expression of leptin and ghrelin, hormones that control appetite and satiety. Gastric leptin, produced by chief and parietal cells and released in response to meals, may play a role in weight gain after eradication of H. pylori infection, whereas ghrelin, produced by X/A-like enteroendocrine cells in oxyntic gland, is released during fasting, and suppressed by feeding and leptin. Whether either that H. pylori genes represent microbial contributions to the complement of thrifty genes of humans, or that H. pylori disappearance plays a role in adiposity remains to be determined. Simply, ghrelin-leptin might tango in body weight regulation, gastric inflammation, and gastric motility. In the current review about the possible role of ghrelin in gastric inflammation, we found that high serum albumin condition decreased ghrelin expression, whereas serum albumin deprivation significantly increased ghrelin expression, however, of which regulation was abolished after H. pylori infection. Ghrelin significantly attenuated the inflammatory stimuli imposed after H. pylori, shown with inactivation of phospho-extracellular signal-regulated kinase (p-ERK) and nuclear factor-KappaB (NF-KappaB)-DNA binding activities. Conclusively, besides orexigenic and weight gaining actions of gastric hormone, ghrelin, it likely endows the stomach the protective effect from exogenous damages.
Amino Acid Sequence ; Appetite Stimulants ; Gastritis/*metabolism/microbiology ; Ghrelin/*blood/chemistry ; Helicobacter Infections/*metabolism ; *Helicobacter pylori ; Humans ; Insulin-Like Growth Factor I/analysis ; Leptin/*blood ; Mitogen-Activated Protein Kinases/metabolism ; Molecular Sequence Data ; NF-kappa B/metabolism ; Neurosecretory Systems/*metabolism ; Peptide Hormones/*blood ; Signal Transduction ; Weight Gain