scholarly journals IL CONTROLLO NEUROENDOCRINO DEL COMPORTAMENTO ALIMENTARE

2020 ◽  
Author(s):  
Francesco Cavagnini
Keyword(s):  
Gastrointestinal Tract ◽  
Food Intake ◽  
Nutritional Status ◽  
Eating Behavior ◽  
Nucleus Tractus Solitarius ◽  
Peptide Yy ◽  
Releasing Hormone ◽  
Fat Depots ◽  
Adiposity Signals ◽  
The Brain

Appetite is regulated by a complex system of central and peripheral signals that interact in order to modulate eating behavior according the individual needs, i.e. the fasting or fed condition and the general nutritional status. Peripheral regulation includes adiposity signals and satiety signals, while central control is accomplished by several effectors, including the neuropeptidergic, monoaminergic and endocannabinoid systems. Adiposity signals inform the brain of the general nutritional status of the subject as indicated by the extent of fat depots. Indeed, leptin produced by the adipose tissue and insulin, whose pancreatic secretion tends to increase with the increase of fat mass, convey to the brain an anorexigenic message. Satiety signals, including cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), originate from the gastrointestinal tract during a meal and, through the vagus nerve, reach the nucleus tractus solitarius (NTS) in the caudal brainstem. From NTS afferents fibers project to the arcuate nucleus (ARC) of the hypothalamus, where satiety signals are integrated with adiposity signals and with several hypothalamic and supra-hypothalamic inputs, thus creating a complex network of neural circuits that finally elaborate the most appropriate response, in terms of eating behavior. In more detail, ARC neurons secrete a number of neuropeptides with orexigenic properties, such as neuropeptide Y (NPY) and agouti-related peptide (AGRP), or anorexigenic effects such as pro-opiomelanocortin (POMC) and cocaine- and amphetamine-regulated transcript (CART). Other brain areas involved in the control of food intake are located downstream the ARC: among these, the paraventricular nucleus (PVN), which produces anorexigenic peptides such as thyrotropin releasing hormone (TRH), corticotrophin releasing hormone (CRH) and oxytocin, the lateral hypothalamus (LHA) and perifornical area (PFA), secreting the orexigenic substances orexin-A (OXA) and melanin concentrating hormone (MCH). Recently, a great interest has developed for endogenous cannabinoids, important players in the regulation of food intake and energy metabolism. In the same context, increasing evidence is accumulating for a role played by the microbiota, the trillion of microorganism populating the human gastrointestinal tract. The complex interaction between the peripheral organs and the central nervous system has generated the concept of gut-brain axis, now incorporated into the physiology. A better understanding of the mechanisms governing the eating behavior will allow the development of drugs capable of reducing or enhancing food consumption.

Central nervous control of voluntary food intake

1989 ◽  
Vol 13 ◽  
pp. 7-26 ◽  
Author(s):  
J. M. Forbes ◽  
J. E. Blundell
Keyword(s):  
Nervous System ◽  
Food Intake ◽  
Peptide Yy ◽  
Blood Stream ◽  
Vital Role ◽  
Nervous Control ◽  
Electrolytic Lesions ◽  
The Central Nervous System ◽  
The Brain ◽  
Voluntary Food Intake

AbstractThe central nervous system is the integrator of most of the actions of the animal and as such plays a vital rôle in the control of voluntary food intake. Much of the work to understand how intake is controlled has been carried out with rats but that which has been done with pigs is included. The first experiments used electrolytic lesions in the designation of the ‘hunger centre’ and the ‘satiety centre’. Recent work has identified the paraventricular nucleus as a sensing site for experimental manipulations. Chemical stimulation of the brain has also been carried out to try to gain understanding of the rôle of neurotransmitters. Noradrenaline (NA) stimulates intake when given into many sites. Serotonin (5-HT) inhibits intake and has been claimed to play a rôle in the selection of macronutrients but 5-HT must now be interpreted in the light of the existence of several different subtypes of 5-HT receptors. Dopamine appears to moderate the hedonic response of eating. Numerous peptides are active in the brain where their rôle as neuromodulators may be quite different from their function in the periphery and at least three types of opioid receptors are implicated with kappa antagonists producing the most potent facilitatory effects. Neuropeptide Y and peptide YY produce massive orexigenic effects which readily overcome peripheral satiety factors. The brain cannot control intake in isolation. It receives inputs in the blood stream, such as glucose, as well as via the nervous system, both from the special senses and from visceral organs such as stomach, intestines and liver. Taste and olfaction are important in diet selection and a specific appetite for protein has been demonstrated in the pig.

Gastrointestinal Satiety Signals III. Glucagon-like peptide 1, oxyntomodulin, peptide YY, and pancreatic polypeptide

2004 ◽  
Vol 286 (5) ◽  
pp. G693-G697 ◽  
Author(s):  
Sarah Stanley ◽  
Katie Wynne ◽  
Steve Bloom
Keyword(s):  
Gastrointestinal Tract ◽  
Animal Models ◽  
Eating Behavior ◽  
Pancreatic Polypeptide ◽  
Peptide Yy ◽  
Gastrointestinal Function ◽  
L Cells ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Many peptides are synthesized and released from the gastrointestinal tract and pancreas, including pancreatic polypeptide (PP) and the products of the gastrointestinal L cells, glucagon-like peptide 1 (GLP-1), oxyntomodulin, and peptide YY (PYY). Whereas their roles in regulation of gastrointestinal function have been known for some time, it is now evident that they also influence eating behavior. This review considers the anorectic peptides PYY, PP, GLP-1, and oxyntomodulin, which decrease appetite and promote satiety in both animal models and humans.

scholarly journals SAT-603 Growth Hormone-Releasing Hormone (GHRH) Antagonists Stimulate Feeding in Mice

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Sheila Leone ◽  
Lucia Recinella, PharmD ◽  
Annalisa Chiavaroli, PharmD ◽  
Giustino Orlando, PharmD ◽  
Claudio Ferrante, PharmD ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Body Weight ◽  
Locomotor Activity ◽  
Food Intake ◽  
Brown Fat ◽  
Growth Hormone Releasing Hormone ◽  
Antitumor Effects ◽  
Releasing Hormone ◽  
Fat Depots

Abstract Growth hormone-releasing hormone (GHRH) is a hypothalamic neuropeptide which stimulates the synthesis and secretion of growth hormone (GH) in pituitary gland. GHRH was also found to modulate food intake in mammals. MIA-690 is a synthetic GHRH antagonist of the Miami (MIA) series with potent antitumor effects. To date, its role in hypothalamic feeding modulation has not been evaluated. In the present study, we aimed to investigate the effects of chronic MIA-690 administration on feeding behavior, locomotor activity and hypothalamic dopamine (DA), norepinephrine (NE), serotonin (5-hydroxytriptamine, 5-HT), orexigenic peptides [agouti-related peptide (AgRP) and neuropeptide Y (NPY)] and anorexigenic peptides [cocaine and amphetamine-regulated transcript (CART) and proopiomelanocortin (POMC)] activity. Adult C57/BL6 mice were treated daily for 4 weeks by subcutaneous administration of (5 µg) MIA-690 or vehicle solution. Food intake and body weight were recorded every 4 days throughout the study. Immediately after the last injection, locomotor activity in the home cage was recorded, and thereafter animals were sacrificed. Visceral, subcutaneous and brown fat depots were quickly excised and weighed. Hypothalamus was also dissected for evaluating gene expression of AgRP, NPY, CART and POMC by real-time reverse transcription polymerase chain reaction. In addition, hypothalamic DA, NE and 5-HT levels were measured by high performance liquid chromatography (HPLC) coupled to electrochemical detection. Our findings show that administration of MIA-690 increased food intake and body weight, without affecting locomotor activity. No difference was observed in visceral, subcutaneous and brown fat mass in animals treated with MIA-690 or vehicle. As for neuromodulatory effects, a significant increase of AgRP gene expression and NE levels, along with a reduction of 5-HT levels were found after MIA-690 treatment. On the other hand, we did not observe any alteration in NPY, POMC and CART gene expression, as well as DA levels, following MIA-690 administration. In conclusion, chronic peripheral administration of MIA-690 could play an orexigenic role paralleled by increased body weight. The stimulation of feeding could be mediated, at least in part, by increased AgRP gene expression and NE levels and decreased 5-HT levels, in the hypothalamus.

scholarly journals Some biological aspects of partial starvation. The effect of weight loss and regrowth on body compsition in sheep

1974 ◽  
Vol 32 (3) ◽  
pp. 515-527 ◽  
Author(s):  
J. H. Burton ◽  
M. Anderson ◽  
J. T. Reid
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Gastrointestinal Tract ◽  
Food Intake ◽  
Energy Content ◽  
Normal Growth ◽  
Whole Body ◽  
Tissue Samples ◽  
Fat Depots ◽  
Dietary Treatments

1. A study of the effects of four dietary treatments on body-weight and the water, protein, fat and energy content of the empty bodies of forty-three Suffolk ewes is reported. The treatments were as follows: T1, ad lib. food intake from a full-body-weight (FBW) of 40 kg to 71 kg; T2, partial fasting with a resulting weight loss from 71 kg to 50 kg FBW; T3, realimentation and regrowth from 50 kg to 71 kg FBW; T4, a slight food restriction producing a reduced growth rate from 40 kg to 50 kg FBW followed by ad lib. food intake from 50 kg to 71 kg FBW. On all treatments sheep were slaughtered in groups of three at 7 kg intervals between 50 kg and 71 kg FBW.2. The whole body, with the exception of several body organs and glands, wool and the contents of the gastrointestinal tract, was minced and analysed for water, protein, fat and energy. Adipose tissue samples were removed at slaughter from subcutaneous and internal fat depots for histological examination. Regression analysis was used in comparing treatment effects on body composition.3. No significant differences were observed between the results of T1 and T4. In consequence these results were pooled and are referred to as T1. At 40 kg FBW the empty (ingesta-free) bodies of the lambs contained approximately 52% water, 14 % protein and 29% fat. Through normal growth to 71 kg FBW on T1 these values had changed to 40, 11.5 and 45 %, respectively. Following weight loss to 50 kg FBW on T2 the water, protein and fat contents of the empty bodies were 47, 13.5 and 35 %, respectively. Regrowth on T3 to 71 kg FBW resulted in little change in these components, the respective values being 46, 13 and 36 %. The sheep which had undergone weight loss and regrowth retained significantly more water and less energy than normally grown controls and tended to deposit less fat and more protein.4. Gastrointestinal tract contents accounted for 11 % of FBW at 71 kg in T3 animals. In T1, the value was 7.1 % at a similar FBW. Thus there was an average increase of over 56 % in contents in the realimented animals.5. Mean adipocyte diameter at 50 kg FBW on T1 was 134 ± 3 μm. At 71 kg FBW the mean diameter had increased to 152 ± 9 μm. Weight reduction (T2) and regrowth (T3) resulted in mean diameters of 122 ± 4 μm and 143 ± 4 μm at 50 kg and 71 kg FBW, respectively.

scholarly journals Obesity and Appetite Control

2012 ◽  
Vol 2012 ◽  
pp. 1-19 ◽  
Author(s):  
Keisuke Suzuki ◽  
Channa N. Jayasena ◽  
Stephen R. Bloom
Keyword(s):  
Food Intake ◽  
Energy Homeostasis ◽  
Peptide Yy ◽  
Gut Hormones ◽  
Appetite Control ◽  
Control Food ◽  
Adiposity Signals ◽  
Term Energy ◽  
Glucagon Like Peptide 1 ◽  
Control Food Intake

Obesity is one of the major challenges to human health worldwide; however, there are currently no effective pharmacological interventions for obesity. Recent studies have improved our understanding of energy homeostasis by identifying sophisticated neurohumoral networks which convey signals between the brain and gut in order to control food intake. The hypothalamus is a key region which possesses reciprocal connections between the higher cortical centres such as reward-related limbic pathways, and the brainstem. Furthermore, the hypothalamus integrates a number of peripheral signals which modulate food intake and energy expenditure. Gut hormones, such as peptide YY, pancreatic polypeptide, glucagon-like peptide-1, oxyntomodulin, and ghrelin, are modulated by acute food ingestion. In contrast, adiposity signals such as leptin and insulin are implicated in both short- and long-term energy homeostasis. In this paper, we focus on the role of gut hormones and their related neuronal networks (the gut-brain axis) in appetite control, and their potentials as novel therapies for obesity.

scholarly journals SAT-605 Characterization of Dual Projection Patterns of Refeeding-Activated Neurons in the Parasubthalamic Nucleus

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Gabor Wittmann ◽  
Nicholas Cosentino ◽  
Ronald M Lechan
Keyword(s):  
Food Intake ◽  
Nucleus Tractus Solitarius ◽  
Brain Regions ◽  
Central Nucleus ◽  
Free Access ◽  
Target Area ◽  
Sprague Dawley ◽  
Bed Nucleus ◽  
Alexa Fluor ◽  
The Brain

Abstract We have observed that following a fast, animals terminate their food intake within 2h after refeeding accompanied by a pattern of neuronal activation as identified by c-fos immunostaining that involves a number of brain regions associated with the regulation of food intake including the nucleus tractus solitarius (NTS), parabrachial nucleus (PBN), central nucleus of the amygdala (CEA), hypothalamic arcuate and paraventricular nuclei, and bed nucleus of the stria terminalis. We also observed striking c-fos activation in the posterior-lateral hypothalamus called the parasubthalamic nucleus or PSTN, raising the possibility that it may also be an important anorectic center in the brain. To establish how the PSTN is integrated into the CNS, we performed dual-label retrograde tract tracing studies to characterize whether refeeding-activated PSTN neurons project to one, or more than one target area in the CNS. Adult, Sprague-Dawley rats received dual stereotaxic injections of Alexa Fluor 488- and Alexa Fluor 555-conjugated cholera toxin β subunit (CTB; 0.1%, 0.5–1 µl volume) into the 1) PBN and NTS, 2) PBN and CEA and 3) NTS and CEA. After 7–12 days, the animals were fasted for 24 h and then given free access to food for 2 h before euthanasia by transcardial perfusion with 4% paraformaldehyde. Brains with successful dual injections were further processed for c-fos immunohistochemistry. The results showed that 26.5±3.8% of PSTN neurons projecting to the PBN also project to the CEA, and 34.6±7.6% of PSTN neurons that project to the CEA also project to the PBN. In addition, 20.2±2.7% of PSTN neurons that project to the PBN also project to the NTS, and 38.1±9.7% of PSTN neurons that project to the NTS also project to the PBN. Furthermore, 35.0±12.5% of PSTN neurons that project to the CEA project to the NTS and 37.1±4.0% of PSTN neurons that project to the NTS project to the CEA. Finally, up to 15% of the neurons with dual projections to the PBN and CEA contained c-fos after refeeding; up to 18% of the neurons with dual projections to the PBN and NTS contained c-fos; and up to 30% of neurons with dual projections to the NTS and CEA contained c-fos. We conclude that a large number of PSTN neurons have more than one projection site within the brain, thus the PSTN appears to have the capability of simultaneously communicating information about appetite to several, major feeding-related sites within the brain, presumably to terminate feeding.

scholarly journals The Role of “Mixed” Orexigenic and Anorexigenic Signals and Autoantibodies Reacting with Appetite-Regulating Neuropeptides and Peptides of the Adipose Tissue-Gut-Brain Axis: Relevance to Food Intake and Nutritional Status in Patients with Anorexia Nervosa and Bulimia Nervosa

2013 ◽  
Vol 2013 ◽  
pp. 1-21 ◽  
Author(s):  
Kvido Smitka ◽  
Hana Papezova ◽  
Karel Vondra ◽  
Martin Hill ◽  
Vojtech Hainer ◽  
...  
Keyword(s):  
Eating Disorders ◽  
Adipose Tissue ◽  
Food Intake ◽  
Bulimia Nervosa ◽  
Eating Behavior ◽  
Peptide Yy ◽  
Abnormal Eating ◽  
Normal Body Weight ◽  
Circulating Autoantibodies ◽  
The Individual

Eating disorders such as anorexia (AN) and bulimia nervosa (BN) are characterized by abnormal eating behavior. The essential aspect of AN is that the individual refuses to maintain a minimal normal body weight. The main features of BN are binge eating and inappropriate compensatory methods to prevent weight gain. The gut-brain-adipose tissue (AT) peptides and neutralizing autoantibodies play an important role in the regulation of eating behavior and growth hormone release. The mechanisms for controlling food intake involve an interplay between gut, brain, and AT. Parasympathetic, sympathetic, and serotoninergic systems are required for communication between brain satiety centre, gut, and AT. These neuronal circuits include neuropeptides ghrelin, neuropeptide Y (NPY), peptide YY (PYY), cholecystokinin (CCK), leptin, putative anorexigen obestatin, monoamines dopamine, norepinephrine (NE), serotonin, and neutralizing autoantibodies. This extensive and detailed report reviews data that demonstrate that hunger-satiety signals play an important role in the pathogenesis of eating disorders. Neuroendocrine dysregulations of the AT-gut-brain axis peptides and neutralizing autoantibodies may result in AN and BN. The circulating autoantibodies can be purified and used as pharmacological tools in AN and BN. Further research is required to investigate the orexigenic/anorexigenic synthetic analogs and monoclonal antibodies for potential treatment of eating disorders in clinical practice.

Insulin and leptin: dual adiposity signals to the brain for the regulation of food intake and body weight

1999 ◽  
Vol 848 (1-2) ◽  
pp. 114-123 ◽  
Author(s):  
Denis G. Baskin ◽  
Dianne Figlewicz Lattemann ◽  
Randy J. Seeley ◽  
Stephen C. Woods ◽  
Daniel Porte ◽  
...  
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Adiposity Signals ◽  
The Brain

scholarly journals Mandatory assessment of trophological status and nutrition in children in drugs prescribing

2020 ◽  
pp. 4-14
Author(s):  
L. A. Kharitonovа ◽  
A. M. Zaprudnov ◽  
K. I. Grigoriev
Keyword(s):  
Trace Elements ◽  
Gastrointestinal Tract ◽  
Food Intake ◽  
Nutritional Status ◽  
The Body ◽  
Malabsorption Syndrome ◽  
Food Ingredients ◽  
Antibiotic Associated Diarrhea ◽  
Active Substances ◽  
Essential Food

The article discusses interactions between medications (Ms) and food. The influence of Ms on the processes of absorption of the essential food ingredients, vitamins, macro- and trace elements in the gastrointestinal tract is analyzed. The significance of the malabsorption syndrome, antibiotic-associated diarrhea as cause of the impaired nutritional status is emphasized. Simultaneously, food products are able of altering the pharmacological effect of some most common drugs. Administration of Ms depending on food intake is discussed. The importance of taking into consideration the influence of foods and theirbiologically active substances on the pharmacokinetics of Ms in the body is pointed out.

scholarly journals Effect of peripheral administration of cholecystokinin on food intake in apolipoprotein AIV knockout mice

2012 ◽  
Vol 302 (11) ◽  
pp. G1336-G1342 ◽  
Author(s):  
Go Yoshimichi ◽  
Chunmin C. Lo ◽  
Kellie L. K. Tamashiro ◽  
Liyun Ma ◽  
Dana M. Lee ◽  
...  
Keyword(s):  
Gene Expression ◽  
Food Intake ◽  
Food System ◽  
Nucleus Tractus Solitarius ◽  
Wild Type ◽  
Post Hoc Analysis ◽  
Nodose Ganglia ◽  
Post Hoc ◽  
The Brain

Apolipoprotein AIV (apo AIV) and cholecystokinin (CCK) are satiation factors secreted by the small intestine in response to lipid meals. Apo AIV and CCK-8 has an additive effect to suppress food intake relative to apo AIV or CCK-8 alone. In this study, we determined whether CCK-8 (1, 3, or 5 μg/kg ip) reduces food intake in fasted apo AIV knockout (KO) mice as effectively as in fasted wild-type (WT) mice. Food intake was monitored by the DietMax food system. Apo AIV KO mice had significantly reduced 30-min food intake following all doses of CCK-8, whereas WT mice had reduced food intake only at doses of 3 μg/kg and above. Post hoc analysis revealed that the reduction of 10-min and 30-min food intake elicited by each dose of CCK-8 was significantly larger in the apo AIV KO mice than in the WT mice. Peripheral CCK 1 receptor (CCK1R) gene expression (mRNA) in the duodenum and gallbladder of the fasted apo AIV KO mice was comparable to that in WT mice. In contrast, CCK1R mRNA in nodose ganglia of the apo AIV KO mice was upregulated relative to WT animals. Similarly, upregulated CCK1R gene expression was found in the brain stem of apo AIV KO mice by in situ hybridization. Although it is possible that the increased satiating potency of CCK in apo AIV KO mice is mediated by upregulation of CCK 1R in the nodose ganglia and nucleus tractus solitarius, additional experiments are required to confirm such a mechanism.

Sign in / Sign up

Export Citation Format

Share Document