BACKGROUND/OBJECTIVES: Cholecystokinin (CCK), a hormone or neuropeptide, is secreted in response to intraluminal nutrients by enteroendocrine I-cells of the intestine and has important physiological actions related to appetite regulation and satiety. The stimulation on CCK secretion from the intestine is of potential relevance for body weight management. Naringenin (4',5,7-trihydroxyflavanone) and its glycoside naringin (naringenin 7-rhamnoglucoside) have been reported to have many biological functions. In the current study, we investigated the question of whether naringenin and naringin could stimulate CCK secretion and then examined the mechanisms involved in CCK release. MATERIALS/METHODS: STC-1 cells were used as a model of enteroendocrine cells. CCK release and changes in intracellular Ca2+ ([Ca2+]i) were measured after incubation of cells with naringenin and naringin for 1 h. RESULTS: Naringenin caused significant (P < 0.05) stimulation of CCK secretion, but naringin did not. In addition, regarding the secretory mechanisms, naringenin-induced CCK secretion involved increases in [Ca2+]i, influx of extracellular Ca2+, at least in part, and activation of TRP channels, including TRPA1. CONCLUSION: Findings of this study suggest that naringenin could have a role in appetite regulation and satiety.
Appetite ; Appetite Regulation ; Body Weight ; Cholecystokinin* ; Enteroendocrine Cells ; Intestines ; Neuropeptides

Recently, obesity has become a worldwide public health concern and the use of anorectic drugs has drastically increased. In this study, sibutramine and phendimetrazine, representative marketed anorectics, were repeatedly administered per os on a daily basis into C57BL/6 mice and the effects of these drugs on food intakes, body weight changes and gene expression profiles were monitored for up to following 7 days. Methamphetamine, which has a potent anorectic effect, was used as a positive control. Anorectic effects were sustained only for two days by phendimetrazine or methamphetamine, but for six days by sibutramine. The modulations of gene expressions in the hypothalamus and the striatum were investigated using microarrays on day 2 and day 7 post-administration, which corresponded to the anorectic period and a return of appetite respectively, for all three drugs tested. Differences in overall gene expression profiles in the stratum on day 2 for sibutramine and phendimetrazine seems to reflect difference between the two in terms of the onsets of drug tolerance. According to microarray findings, the Ankrd26 gene appears to have an important anorectic role, whereas the up-regulation of the olfaction system appeared to be involved in the drug tolerance of anorectics. The microarray data presented in this study demonstrates the usefulness of gene expression analysis for gathering information on the efficacy and safety of anorectic drugs.
Animals ; Appetite ; Appetite Depressants ; Body Weight Changes ; Cyclobutanes ; Drug Tolerance ; Gene Expression ; Gene Expression Profiling ; Hypothalamus ; Methamphetamine ; Mice ; Morpholines ; Obesity ; Public Health ; Smell ; Transcriptome ; Up-Regulation

The prevalence of obesity has been rapidly increasing worldwide over the last several decades and has become a major health problem in developed countries. The brain, especially the hypothalamus, plays a key role in the control of food intake by sensing metabolic signals from peripheral organs and modulating feeding behaviors. To accomplish these important roles, the hypothalamus communicates with other brain areas such as the brainstem and reward-related limbic pathways. The adipocyte-derived hormone leptin and pancreatic beta-cell-derived insulin inform adiposity to the hypothalamus. Gut hormones such as cholecystokinin, peptide YY, pancreatic polypeptide, glucagon-like peptide 1, and oxyntomodulin transfer satiety signals to the brain and ghrelin relays hunger signals. The endocannabinoid system and nutrients are also involved in the physiological regulation of food intake. In this article, we briefly review physiological mechanisms of appetite regulation.
Adiposity ; Appetite ; Appetite Regulation ; Brain ; Brain Stem ; Cholecystokinin ; Developed Countries ; Eating ; Endocannabinoids ; Feeding Behavior ; Ghrelin ; Glucagon-Like Peptide 1 ; Hunger ; Hypothalamus ; Insulin ; Leptin ; Obesity ; Oxyntomodulin ; Pancreatic Polypeptide ; Peptide YY ; Prevalence

Fenfluramine is an amphetamine-derived substance first developed in the late 1960s for appetite control. Because of its known side effects at therapeutic doses, it is now controlled by the government and has been withdrawn from the market, but the underground market is still big. When over-dosed, it can produce a wide range of neurologic and cardiovascular symptoms, and even death, when a large amount is ingested. We report two cases of acute fenfluramine overdose: a fatal case with generalized seizure and pulseless electrical activity, and a case of relatively mild intoxication.
Appetite ; Fenfluramine* ; Seizures

No abstract available.
Appetite* ; Ghrelin* ; Growth Hormone*

No abstract available.
Appetite* ; Ghrelin* ; Growth Hormone*

BACKGROUND AND OBJECTIVES: Recently, obesity has become one of the major health problems in our society. To overcome this problem, keeping a balance between food intake and energy expenditure is very important. Many natural substances including essential oils have been suggested for their potential effect on reducing weight. This study was performed to evaluate whether aroma inhalation of essential oil has a role in appetite regulation and works on the central nervous system through the olfactory stimulus. MATERIALS AND METHOD: Food intake was measured after 30 minutes of treatment with essential oil in overnight fasted Sprague-Dawley rats. In the control group, saline was used instead of essential oil. Changes in pro-opiomelanocortin (POMC) and neuropeptide Y (NPY) mRNA expression levels in the hypothalamus were measured following 30 minutes of treatment with geranium essential oil using real-time polymerase chain reaction. RESULTS: Of the seven essential oils, geranium significantly decreased the amount of food intake compared to the control group. Geranium essential oil significantly increased POMC mRNA expression in the hypothalamus, but did not change the NPY mRNA expression. The increased POMC mRNA expression was reversed by treatment with xylocaine, which blocks the olfactory perception. CONCLUSION: These results suggest that geranium essential oil has anorexic effect through the activation of POMC neurons in the hypothalamus via olfactory stimulus.
Appetite Regulation ; Central Nervous System ; Diethylpropion ; Eating ; Energy Metabolism ; Geranium ; Hypothalamus ; Inhalation ; Lidocaine ; Neurons ; Neuropeptide Y ; Obesity ; Oils, Volatile ; Olfactory Perception ; Pro-Opiomelanocortin ; Rats, Sprague-Dawley ; RNA, Messenger

Study the infect of child anorexia granule on serum ghrelin and leptin of anorexia children and its clinical efficacy. Selected 81 cases of anorexia children aged 1-6 years old into treatment group (42 cases) and control group (39 cases), in addition, 30 case healthy children as healthy control group. The control group children were treated with domperidone suspension 0.3 mg x kg(-1) x d(-1), tid, orally 30 minutes before meals. Treatment group were treated with child anorexia granule, 1-3 years 1 package, bid; 4-6 years 1 package, tid; po, 4 weeks as a course of treatment. Study the change of serum ghrelin and leptin before and after therapy. The study demonstrates that before treatment, the serum ghrelin level of disease group was lower than healthy group (P < 0.01), and the serum leptin level was higher than healthy group (P < 0.01). After treatment, the serum ghrelin level both increase, and the serum leptin decline. And the change of treatment group was significantly different with control group (P < 0.01). And the clinical effective rate are 95.23% and 74.35% (P < 0.01). After 6 months of follow-up visit, the children weight significantly increase in treatment group (P < 0.01). Results indicate that child anorexia granule can facilitate secretion of ghrelin, and inhibit secretion of leptin, so as to work up an appetite. And the molecular mechanism is its infect on serum ghrelin, leptin.
Anorexia ; drug therapy ; metabolism ; physiopathology ; Appetite Regulation ; drug effects ; Body Weight ; drug effects ; Child ; Child, Preschool ; Drugs, Chinese Herbal ; administration & dosage ; Female ; Ghrelin ; metabolism ; Humans ; Infant ; Leptin ; metabolism ; Male

The release of hormones and the metabolism of human body are controlled by the circadian rhythm related to sleep-wake cycle. Growth hormone, prolactin, thyroid stimulating hormone, cortisol, glucose, and insulin-secretion rates fluctuate according to the sleep-wake cycle. In addition, sleep is related to the appetite regulation and carbohydrate and other energy metabolism. Hypocretin (orexin), an excitatory neuropeptide, regulates waking and diet intake, and the poor sleep increases diet intake. The short sleep duration increases one's body mass index and impairs the function of the endocrine and metabolism, causing increases in the risk of glucose intolerance and diabetes. The poor sleep quality and sleep disorders have similar impact on the metabolic function. In short, the sleep loss and the poor quality of sleep have a detrimental effect on the endocrine and energy metabolism. The improvement of sleep quality by the future research and appropriate clinical treatment would contribute to the decrease of the metabolic diseases such as diabetes.
Appetite Regulation ; Body Mass Index ; Circadian Rhythm ; Diet ; Energy Metabolism ; Glucose ; Glucose Intolerance ; Growth Hormone ; Human Body ; Hydrocortisone ; Intracellular Signaling Peptides and Proteins ; Metabolic Diseases ; Neuropeptides ; Prolactin ; Sleep Wake Disorders ; Thyrotropin ; Orexins

Ghrelin is a 28-amino-acid peptide that plays multiple roles in humans and other mammals. The functions of ghrelin include food intake regulation, gastrointestinal (GI) motility, and acid secretion by the GI tract. Many GI disorders involving infection, inflammation, and malignancy are also correlated with altered ghrelin production and secretion. Although suppressed ghrelin responses have already been observed in various GI disorders, such as chronic gastritis, Helicobacter pylori infection, irritable bowel syndrome, functional dyspepsia, and cachexia, elevated ghrelin responses have also been reported in celiac disease and inflammatory bowel disease. Moreover, we recently reported that decreased fasting and postprandial ghrelin levels were observed in female patients with functional dyspepsia compared with healthy subjects. These alterations of ghrelin responses were significantly correlated with meal-related symptoms (bloating and early satiation) in female functional dyspepsia patients. We therefore support the notion that abnormal ghrelin responses may play important roles in various GI disorders. Furthermore, human clinical trials and animal studies involving the administration of ghrelin or its receptor agonists have shown promising improvements in gastroparesis, anorexia, and cancer. This review summarizes the impact of ghrelin, its family of peptides, and its receptors on GI diseases and proposes ghrelin modulation as a potential therapy.
Animals ; Anorexia ; Appetite Regulation ; Cachexia ; Celiac Disease ; Dyspepsia ; Fasting ; Female ; Gastritis ; Gastrointestinal Diseases ; Gastrointestinal Tract ; Gastroparesis ; Ghrelin ; Helicobacter pylori ; Humans ; Inflammation ; Inflammatory Bowel Diseases ; Irritable Bowel Syndrome ; Mammals ; Peptides ; Receptors, Ghrelin