Animals ; Anorexia ; etiology ; Appetite ; physiology ; Cholecystokinin ; physiology ; Digestion ; Glucagon-Like Peptide 1 ; physiology ; Humans ; Hypothalamus ; physiology ; Insulin ; physiology ; Norepinephrine ; physiology

Ghrelin, a novel gastrointestinal peptide with 28 amino acids, is secreted from the A-like cells of the gastric fundus. This peptide hormone does not only promote the release of growth hormone, but also stimulates food intake, gastric motility and cardiac output. Increased plasma ghrelin level has been reported in patients with upper gastrointestinal (GI) disease or in their disease animal model, suggesting its important role in the pathogenesis of upper GI disease.
Appetite/*physiology ; Cysteamine/metabolism ; Dyspepsia/etiology ; *Eating ; Gastrointestinal Diseases/*etiology ; Ghrelin/*physiology ; Humans ; Peptic Ulcer/etiology

Excess energy intake, without a compensatory increase of energy expenditure, leads to obesity. Several molecules are involved in energy homeostasis regulation and new ones are being discovered constantly. Appetite regulating hormones such as ghrelin, peptide tyrosine-tyrosine and amylin or incretins such as the gastric inhibitory polypeptide have been studied extensively while other molecules such as fibroblast growth factor 21, chemerin, irisin, secreted frizzle-related protein-4, total bile acids, and heme oxygenase-1 have been linked to energy homeostasis regulation more recently and the specific role of each one of them has not been fully elucidated. This mini review focuses on the above mentioned molecules and discusses them in relation to their regulation by the macronutrient composition of the diet as well as diet-induced weight loss.
Appetite ; Bile Acids and Salts ; Diet ; Energy Intake ; Energy Metabolism ; Fibroblast Growth Factors ; Gastric Inhibitory Polypeptide ; Ghrelin ; Heme Oxygenase-1 ; Homeostasis* ; Incretins ; Islet Amyloid Polypeptide ; Obesity ; Physiology* ; Weight Loss*

Anorexia nervosa, bulimia and other related eating disorders are a heterogenous group of psychiatric disorders whose prevalence rates reach 0.5-1.0% for anorexia nervosa and 1.0-3.0% for bulinmia nervosa. Anorexia nervosa is characterized by a refusal to maintain a minimally normal body weight and bulimia is characterized by repeated episodes of binge eating, misuse of laxatives. diuretics or other medications ; fasting and excessive exercise. A disturbance in perception of body shape and weight is an essential feature of both disorders. Patients with eating disorders may have numerous medical, hypothalamic endocrine, metabolic and nutritional abnormalities. There have been several conceptual models to explain the etiology of eating disorders These are socio-cultural, family pathological, individual psychodynamic, developmental psychobiologiccl, primary hypothalamic dysfunctional, cognitive-behavioral and affective disorder theories. Among these thoeries, this paper attempts to review the biological theory and pharmacotherapy in eating disorders. Specifically, this review deals with physiology of eating behavior, neurotransmitter regulation of appetite and eating bvehavior, disturbances in brcin neurotransmitter system, neuroendocrine findings in anorexia nervosa and bulimia nervosa. and finally pharmacotherapy. Based on this review, future directions for research are also sutggested.
Anorexia Nervosa ; Appetite ; Biology* ; Bulimia ; Bulimia Nervosa ; Disulfiram ; Diuretics ; Drug Therapy* ; Feeding and Eating Disorders* ; Eating* ; Fasting ; Feeding Behavior ; Humans ; Ideal Body Weight ; Laxatives ; Mood Disorders ; Neurosecretory Systems ; Neurotransmitter Agents ; Physiology ; Prevalence

OBJECTIVETo explore the cause of decreasing intake food of diet-induced obesity resistant (DIO-R) rats.

METHODSFifty male Sprague-dawley (SD) rats were randomly divided into control group and high-fat group and they were fed with basic diet and high-fat diet respectively for 13 weeks. DIO-R and diet-induced obesity (DIO) rats were selected according to their body weight and the quantity of energy intake, then observing the changes of the total food intake, the level of serum leptin and plasma NPY were determined by radioimmunoassay and the contents of the melanocortin receptor-4 (MCR-4) in brain were determined by Western Blot.

RESULTSThe total food intake of DIO-R rats was (1 679.1 +/- 146.8) g. The total food intake of DIO rats was (1 818.4 +/- 148.9) g. The total food intake of DIO-R rats was lower than that of DIO rats (P < 0.05). The level of plasma NPY of DIO-R rats was (795.24 +/- 83.59) ng/L. The level of plasma NPY of DIO rats was (1 007.14 +/- 172.83) ng/L. The level of plasma NPY of DIO-R rats was lower than that of the DIO rats (P < 0.05). The levels of serum leptin of basic, DIO-R and DIO rats was (4.80 +/- 0.75) microg/L, (9.17 +/- 1.19) microg/L and (9.32 +/- 1.04) microg/L. The level of serum leptin of rats in high-fat diet group was increased as compared with the rats in basic diet group, but there was no significant difference between DIO-R and DIO rats (P > 0.05). The levels of brain MCR-4 of basic, DIO-R and DIO rats were (342 +/- 31) mm2, (455 +/- 33) mm2, (355 +/- 30) mm2. High fat diets increased the content of brain MCR-4 in DIO-R rats.

CONCLUSIONDIO-R rats decreased appetite by increasing expression of ob gene to reduce activity of NPY pathway and activate the MCR-4 pathway, and thus inhibit the increase body of weight.

Animals ; Appetite ; physiology ; Blotting, Western ; Body Weight ; physiology ; Brain ; drug effects ; metabolism ; Dietary Fats ; administration & dosage ; Disease Models, Animal ; Energy Intake ; physiology ; Leptin ; blood ; Male ; Neuropeptide Y ; blood ; Obesity ; blood ; etiology ; physiopathology ; Radioimmunoassay ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Receptor, Melanocortin, Type 4 ; metabolism