scholarly journals The Effects of Ghrelin on Energy Balance and Psychomotor Activity in a Goldfish Model: An Overview

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Ki Sung Kang ◽  
Satowa Yahashi ◽  
Kouhei Matsuda
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Emotional Regulation ◽  
Energy Homeostasis ◽  
Biologically Active ◽  
Receptor System ◽  
Psychomotor Activity ◽  
Peripheral Tissues ◽  
Molecular Variants ◽  
Feeding Control

The goldfish (Carassius auratus) has a number of merits as a laboratory animal, and we have extensively identified the mechanisms by which ghrelin regulates food intake in this species. For the first time, we have purified and characterized 11 molecular variants of ghrelin that are present in goldfish intestine and shown that 17-residue ghrelin, the predominant form with n-octanoyl modification, is biologically active and implicated in the regulation of food intake as an endogenous orexigenic factor. Ghrelin and its receptor system are present not only in peripheral tissues such as stomach and intestine, but also in the central nervous system. Recent studies have also revealed that a number of neuropeptides are widely distributed in the brain in key areas of emotional regulation, and their role as modulators of behavioral states is being increasingly recognized. Interestingly, administration of ghrelin induces an orexigenic effect and also modifies locomotor activity, suggesting the involvement of ghrelin in feeding control and regulation of energy balance. Information derived from studies of ghrelin has been increasing, and important results have been obtained from both fish and mammals. Here, we present an overview of the effects of ghrelin on energy balance and psychomotor activity in the goldfish as an animal model. The available data provide an insight into evolutionary background of ghrelin's multiple actions on energy homeostasis in vertebrates.

scholarly journals The Pleiotropic Potential of BDNF beyond Neurons: Implication for a Healthy Mind in a Healthy Body

Life ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 1256
Author(s):  
Maria Carmela Di Rosa ◽  
Stefania Zimbone ◽  
Miriam Wissam Saab ◽  
Marianna Flora Tomasello
Keyword(s):  
Energy Balance ◽  
Energy Homeostasis ◽  
Molecular Mechanisms ◽  
Cellular Level ◽  
Adaptive Responses ◽  
Peripheral Tissues ◽  
The Central Nervous System ◽  
The Many ◽  
Feeding Control ◽  
Healthy Body

Brain-derived neurotrophic factor (BDNF) represents one of the most widely studied neurotrophins because of the many mechanisms in which it is involved. Among these, a growing body of evidence indicates BDNF as a pleiotropic signaling molecule and unveils non-negligible implications in the regulation of energy balance. BDNF and its receptor are extensively expressed in the hypothalamus, regions where peripheral signals, associated with feeding control and metabolism activation, and are integrated to elaborate anorexigenic and orexigenic effects. Thus, BDNF coordinates adaptive responses to fluctuations in energy intake and expenditure, connecting the central nervous system with peripheral tissues, including muscle, liver, and the adipose tissue in a complex operational network. This review discusses the latest literature dealing with the involvement of BDNF in the maintenance of energy balance. We have focused on the physiological and molecular mechanisms by which BDNF: (I) controls the mitochondrial function and dynamics; (II) influences thermogenesis and tissue differentiation; (III) mediates the effects of exercise on cognitive functions; and (IV) modulates insulin sensitivity and glucose transport at the cellular level. Deepening the understanding of the mechanisms exploited to maintain energy homeostasis will lay the groundwork for the development of novel therapeutical approaches to help people to maintain a healthy mind in a healthy body.

scholarly journals Hypothalamic AMPK as a Mediator of Hormonal Regulation of Energy Balance

2018 ◽  
Vol 19 (11) ◽  
pp. 3552 ◽  
Author(s):  
Baile Wang ◽  
Kenneth Cheng
Keyword(s):  
Energy Balance ◽  
Hormonal Regulation ◽  
Energy Homeostasis ◽  
Adenosine Monophosphate ◽  
Acid Oxidation ◽  
Peripheral Tissues ◽  
Adaptive Thermogenesis ◽  
Increase Food Intake ◽  
Regulatory Effects ◽  
Underlying Mechanisms

As a cellular energy sensor and regulator, adenosine monophosphate (AMP)-activated protein kinase (AMPK) plays a pivotal role in the regulation of energy homeostasis in both the central nervous system (CNS) and peripheral organs. Activation of hypothalamic AMPK maintains energy balance by inducing appetite to increase food intake and diminishing adaptive thermogenesis in adipose tissues to reduce energy expenditure in response to food deprivation. Numerous metabolic hormones, such as leptin, adiponectin, ghrelin and insulin, exert their energy regulatory effects through hypothalamic AMPK via integration with the neural circuits. Although activation of AMPK in peripheral tissues is able to promote fatty acid oxidation and insulin sensitivity, its chronic activation in the hypothalamus causes obesity by inducing hyperphagia in both humans and rodents. In this review, we discuss the role of hypothalamic AMPK in mediating hormonal regulation of feeding and adaptive thermogenesis, and summarize the diverse underlying mechanisms by which central AMPK maintains energy homeostasis.

scholarly journals The PACAP/PAC1 Receptor System and Feeding

2021 ◽  
Author(s):  
Keerthana Sureshkumar ◽  
Andrea Saenz ◽  
Syed Muzzammil Ahmad ◽  
Kabirullah Lutfy
Keyword(s):  
Food Intake ◽  
Energy Homeostasis ◽  
Brain Regions ◽  
Regulatory Action ◽  
Laboratory Animals ◽  
Pac1 Receptor ◽  
Receptor System ◽  
Nervous Systems ◽  
Peripheral Nervous Systems

Pituitary adenylyl cyclase activating polypeptide (PACAP) belongs to the vasoactive intestinal polypeptide (VIP)/secretin/glucagon superfamily. PACAP is present in two forms, PACAP-38 and PACAP-27, and binds to three guanine-regulatory (G) protein-coupled receptors (PAC1, VPAC1, and VPAC2). PACAP is expressed in the central and peripheral nervous systems with high PACAP levels found in the hypothalamus, a brain region involved in feeding and energy homeostasis. PAC1 receptors are high-affinity and PACAP-selective receptors, while VPAC1 and VPAC2 receptors show a comparable affinity to PACAP and VIP. PACAP and its receptors are expressed in the central and peripheral nervous systems, with moderate to high expression in the hypothalamus, amygdala, and other limbic structures. Consistent with their expression, PACAP is involved in several physiological responses and pathological states. A growing body of literature suggests that PACAP regulates food intake in laboratory animals. However, there is no comprehensive review of the literature on this topic. Thus, the purpose of this article is to review the literature regarding the role of PACAP and its receptors in food intake regulation and to synthesize how PACAP exerts its anorexic effects in different brain regions. To achieve this goal, we searched PubMed and reviewed 68 articles regarding the regulatory action of PACAP on food intake. Here, we present the literature regarding the effect of exogenous PACAP on feeding and the role of endogenous PACAP in this process. We also provide evidence regarding the effect of PACAP on the homeostatic and hedonic aspects of food intake, the neuroanatomical sites where PACAP exerts its regulatory action, which PACAP receptors may be involved, and the role of various signaling pathways and neurotransmitters in hypophagic effects of PACAP.

Orexin activation precedes increased NPY expression, hyperphagia, and metabolic changes in response to sleep deprivation

2010 ◽  
Vol 298 (3) ◽  
pp. E726-E734 ◽  
Author(s):  
Paulo José Forcina Martins ◽  
Marina Soares Marques ◽  
Sergio Tufik ◽  
Vânia D'Almeida
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Sleep Deprivation ◽  
Weight Control ◽  
Time Course ◽  
Energy Homeostasis ◽  
Negative Energy ◽  
Negative Energy Balance ◽  
Mrna Levels

Several pieces of evidence support that sleep duration plays a role in body weight control. Nevertheless, it has been assumed that, after the identification of orexins (hypocretins), the molecular basis of the interaction between sleep and energy homeostasis has been provided. However, no study has verified the relationship between neuropeptide Y (NPY) and orexin changes during hyperphagia induced by sleep deprivation. In the current study we aimed to establish the time course of changes in metabolite, endocrine, and hypothalamic neuropeptide expression of Wistar rats sleep deprived by the platform method for a distinct period (from 24 to 96 h) or sleep restricted for 21 days (SR-21d). Despite changes in the stress hormones, we found no changes in food intake and body weight in the SR-21d group. However, sleep-deprived rats had a 25–35% increase in their food intake from 72 h accompanied by slight weight loss. Such changes were associated with increased hypothalamus mRNA levels of prepro-orexin (PPO) at 24 h followed by NPY at 48 h of sleep deprivation. Conversely, sleep recovery reduced the expression of both PPO and NPY, which rapidly brought the animals to a hypophagic condition. Our data also support that sleep deprivation rapidly increases energy expenditure and therefore leads to a negative energy balance and a reduction in liver glycogen and serum triacylglycerol levels despite the hyperphagia. Interestingly, such changes were associated with increased serum levels of glucagon, corticosterone, and norepinephrine, but no effects on leptin, insulin, or ghrelin were observed. In conclusion, orexin activation accounts for the myriad changes induced by sleep deprivation, especially the hyperphagia induced under stress and a negative energy balance.

scholarly journals Peptides and proteins regulating food intake: a comparative view

2006 ◽  
Vol 56 (4) ◽  
pp. 447-473 ◽  
Author(s):  
Gert Flik ◽  
Mark Huising ◽  
Marnix Gorissen
Keyword(s):  
Energy Metabolism ◽  
Energy Balance ◽  
Food Intake ◽  
Energy Homeostasis ◽  
Regulatory Mechanisms ◽  
Main Site ◽  
Recent Developments ◽  
Hypothalamic Arcuate Nucleus ◽  
Regulate Food Intake ◽  
Central Food

AbstractEnergy homeostasis is under multiple endocrine and neural controls that involve both central and peripheral hormones and neuropeptides. Disorders of energy balance (e.g., obesitas and anorexia nervosa) are caused by subtle dysregulation of these regulatory mechanisms. The hypothalamic arcuate nucleus is a main site of central regulation where two distinct subpopulations of neurons co-express either neuropeptide Y (NPY) and agouti-related protein (AgRP), or proopiomelanocortin (POMC) and cocaine and amphetamine-regulated transcript (CART): the former set of peptides increases food intake; the latter decreases food intake and affect energy metabolism. Key peripheral hormones affecting energy metabolism include cholecystokinin (CCK), leptin and insulin, which decrease food intake, and ghrelin, which increases food intake. CCK and ghrelin regulate food intake in the short term (by affecting meal size), whereas leptin and insulin regulate food intake over longer periods spanning several meals. These signals and their physiology are reasonably well understood in mammals. On the other hand, knowledge on energy metabolism in earlier vertebrates is scant. Recently characterised central food intake regulatory mechanisms in fish suggest that they operate in a manner similar to their mammalian counterparts. Peripheral mechanisms have been poorly studied outside mammals. The recent identification of leptin in several fish species provides new insights and opportunities to enhance our understanding of the regulation of food intake. Comparative analysis of these peripheral mechanisms may shed new light on the function and evolution of the mechanisms controlling energy homeostasis. In this review, we summarise recent developments in understanding of mechanisms and signals that regulate energy balance in mammals, and compare these to what we now know about their orthologues in earlier vertebrates, with a particular focus on bony fishes.

scholarly journals Effects of Naltrexone on Energy Balance and Hypothalamic Melanocortin Peptides in Male Mice Fed a High-Fat Diet

2019 ◽  
Vol 3 (3) ◽  
pp. 590-601 ◽  
Author(s):  
Sunil K Panigrahi ◽  
Kana Meece ◽  
Sharon L Wardlaw
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Energy Homeostasis ◽  
Body Weight Gain ◽  
High Fat ◽  
Melanocortin System ◽  
Endogenous Opioid ◽  
Processing Enzymes ◽  
Agouti Related Protein

Abstract The hypothalamic melanocortin system composed of proopiomelanocortin (POMC) and agouti-related protein (AgRP) neurons plays a key role in maintaining energy homeostasis. The POMC-derived peptides, α-MSH and β-EP, have distinct roles in this process. α-MSH inhibits food intake, whereas β-EP, an endogenous opioid, can inhibit POMC neurons and stimulate food intake. A mouse model was used to examine the effects of opioid antagonism with naltrexone (NTX) on Pomc and Agrp gene expression and POMC peptide processing in the hypothalamus in conjunction with changes in energy balance. There were clear stimulatory effects of NTX on hypothalamic Pomc in mice receiving low- and high-fat diets, yet only transient decreases in food intake and body weight gain were noted. The effects on Pomc expression were accompanied by an increase in POMC prohormone levels and a decrease in levels of the processed peptides α-MSH and β-EP. Arcuate expression of the POMC processing enzymes Pcsk1, Pcsk2, and Cpe was not altered by NTX, but expression of Prcp, an enzyme that inactivates α-MSH, increased after NTX exposure. NTX exposure also stimulated hypothalamic Agrp expression, but the effects of NTX on energy balance were not enhanced in Agrp-null mice. Despite clear stimulatory effects of NTX on Pomc expression in the hypothalamus, only modest transient decreases in food intake and body weight were seen. Effects of NTX on POMC processing, and possibly α-MSH inactivation, as well as stimulatory effects on AgRP neurons could mitigate the effects of NTX on energy balance.

scholarly journals OR04-03 Calcitonin Receptor Expressing Neurons in the PVH Regulate Feeding Behavior

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Ian Enrique Gonzalez ◽  
Wenwen Cheng ◽  
Warren Pan ◽  
Chunxia Lu ◽  
Julliana Ramirez-Matias ◽  
...  
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Feeding Behavior ◽  
Tetanus Toxin ◽  
Energy Homeostasis ◽  
Balance Control ◽  
Brain Regions ◽  
Calcitonin Receptor ◽  
Cumulative Food Intake

Abstract The paraventricular nucleus of the hypothalamus (PVH) is a brain region crucial for energy homeostasis. Abnormal PVH development or damage leads to hyperphagic obesity and energy expenditure deficits underscoring the importance of PVH neuronal activity in energy balance control. Application of salmon calcitonin (sCT) to the PVH suppresses feeding and calcitonin receptor (CalcR) is highly expressed in the PVH of rodents suggesting that CalcR-expressing PVH neurons contribute to energy homeostasis. In situ hybridization reveals that many CalcRPVH neurons express melanocortin-4 receptor (MC4R), a receptor required for normal feeding behavior. To investigate the physiologic roles of CalcRPVH neurons, we generated CalcR-2a-Cre knock-in mice to manipulate CalcR-expressing cells. Deletion of MC4R from CalcR expressing cells using Cre-loxP technology resulted in profound obesity in both male and female mice by 16 weeks of age. This weight gain was attributable to hyperphagia, as cumulative food intake of the MC4R deleted mice was significantly greater than the controls and energy expenditure measurements acquired through CLAMS analysis were not significantly different. To determine the brain regions engaged by CalcRPVH neurons, we used anterograde Cre-dependent viral tracing reagents injected into the PVH of CalcR-Cre mice, and found that CalcRPVH neurons project to brain regions implicated in energy balance control, including the nucleus of the solitary tract and the parabrachial nucleus. To assess the acute effects of activating CalcRPVH neurons, we used DREADD technology to chemogenetically activate CalcRPVH neurons. CalcRPVH neuron activation suppressed feeding but had no significant effect on energy expenditure. To determine if the activity of CalcRPVH neurons is required for energy homeostasis, we silenced them using Cre-dependent tetanus toxin virus. Male mice with tetanus toxin silenced CalcRPVH neurons were obese 7 weeks following injection in part due to greater cumulative food intake; CLAMS analysis revealed no differences in energy expenditure. Mice with silenced CalcRPVH neurons as well as mice with CalcR deleted from the PVH had normal anorectic responses to sCT, suggesting sCT-induced anorexia does not require CalcRPVH neurons or CalcR expression in the PVH. Taken together, these findings suggest CalcRPVH neurons are an essential component of feeding and energy homeostatic circuitry.

scholarly journals The PACAP/PAC1 Receptor System and Feeding

2021 ◽  
Vol 12 (1) ◽  
pp. 13
Author(s):  
Keerthana Sureshkumar ◽  
Andrea Saenz ◽  
Syed M. Ahmad ◽  
Kabirullah Lutfy
Keyword(s):  
Food Intake ◽  
Energy Homeostasis ◽  
Brain Regions ◽  
Regulatory Action ◽  
Laboratory Animals ◽  
Pac1 Receptor ◽  
Receptor System ◽  
Nervous Systems ◽  
Peripheral Nervous Systems

Pituitary adenylyl cyclase activating polypeptide (PACAP) belongs to the vasoactive intestinal polypeptide (VIP)/secretin/glucagon superfamily. PACAP is present in two forms (PACAP-38 and PACAP-27) and binds to three guanine-regulatory (G) protein-coupled receptors (PAC1, VPAC1, and VPAC2). PACAP is expressed in the central and peripheral nervous systems, with high PACAP levels found in the hypothalamus, a brain region involved in feeding and energy homeostasis. PAC1 receptors are high-affinity and PACAP-selective receptors, while VPAC1 and VPAC2 receptors show a comparable affinity to PACAP and VIP. PACAP and its receptors are expressed in the central and peripheral nervous systems with moderate to high expression in the hypothalamus, amygdala, and other limbic structures. Consistent with their expression, PACAP is involved in several physiological responses and pathological states. A growing body of literature suggests that PACAP regulates food intake in laboratory animals. However, there is no comprehensive review of the literature on this topic. Thus, the purpose of this article is to review the literature regarding the role of PACAP and its receptors in food intake regulation and to synthesize how PACAP exerts its anorexic effects in different brain regions. To achieve this goal, we searched PubMed and reviewed 68 articles regarding the regulatory action of PACAP on food intake. Here, we present the literature regarding the effect of exogenous PACAP on feeding and the role of endogenous PACAP in this process. We also provide evidence regarding the effect of PACAP on the homeostatic and hedonic aspects of food intake, the neuroanatomical sites where PACAP exerts its regulatory action, which PACAP receptors may be involved, and the role of various signaling pathways and neurotransmitters in hypophagic effects of PACAP.

scholarly journals A high-protein total diet replacement alters the regulation of food intake and energy homeostasis in healthy, normal-weight adults

2021 ◽  
Author(s):  
Camila L. P. Oliveira ◽  
Normand G. Boulé ◽  
Sarah A. Elliott ◽  
Arya M. Sharma ◽  
Mario Siervo ◽  
...  
Keyword(s):  
Energy Balance ◽  
Food Intake ◽  
Weight Control ◽  
Energy Homeostasis ◽  
Normal Weight ◽  
High Protein ◽  
Whole Body ◽  
Blood Levels ◽  
Total Diet ◽  
The Impact

Abstract Purpose Dietary intake can affect energy homeostasis and influence body weight control. The aim of this study was to compare the impact of high-protein total diet replacement (HP-TDR) versus a control (CON) diet in the regulation of food intake and energy homeostasis in healthy, normal-weight adults. Methods In this acute randomized controlled, cross-over study, participants completed two isocaloric arms: a) HP-TDR: 35% carbohydrate, 40% protein, and 25% fat; b) CON: 55% carbohydrate, 15% protein, and 30% fat. The diets were provided for 32 h while inside a whole-body calorimetry unit. Appetite sensations, appetite-related hormones, and energy metabolism were assessed. Results Forty-three healthy, normal-weight adults (19 females) participated. Appetite sensations did not differ between diets (all p > 0.05). Compared to the CON diet, the change in fasting blood markers during the HP-TDR intervention was smaller for peptide tyrosine-tyrosine (PYY; − 18.9 ± 7.9 pg/mL, p = 0.02) and greater for leptin (1859 ± 652 pg/mL, p = 0.007). Moreover, postprandial levels of glucagon-like peptide 1 (1.62 ± 0.36 pM, p < 0.001) and PYY (31.37 ± 8.05 pg/mL, p < 0.001) were higher in the HP-TDR. Significant correlations were observed between energy balance and satiety (r = − 0.41, p = 0.007), and energy balance and PFC (r = 0.33, p = 0.033) in the HP-TDR. Conclusion Compared to the CON diet, the HP-TDR increased blood levels of anorexigenic hormones. Moreover, females and males responded differently to the intervention in terms of appetite sensations and appetite-related hormones. Trial registration NCT02811276 (retrospectively registered on 16 June 2016) and NCT03565510 (retrospectively registered on 11 June 2018).

The Plasma Concentrations of the Anorexigenic PYY and Orexigenic Ghrelin Decrease and Increase Respectively during Chemotherapy in Children with Acute Lymphoblastic Leukaemia, as the Leukemic Burden Is Gradually Eliminated and the Body Weight Improves.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4541-4541
Author(s):  
Maria Moschovi ◽  
Maria Vounatsou ◽  
Ioannis Papassotiriou ◽  
George P. Chrousos ◽  
Fotini Tzortzatou-Stathopoulou
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Acute Lymphoblastic Leukaemia ◽  
Lymphoblastic Leukaemia ◽  
Endocrine Cells ◽  
Plasma Concentrations ◽  
Maintenance Phase ◽  
The Body ◽  
Peripheral Tissues

Abstract Anorexia and cachexia are common manifestations in children with acute lymphoblastic leukaemia (ALL) at diagnosis. Possible mediators of the anorexia-cachexia syndrome are hormones, cytokines, and adipokines from peripheral tissues, and neurotransmitters, neuropeptides, cytokines, and other hormones in the hypothalamus. Peptide YY (PYY) and ghrelin are gastrointestinal track-derived hormones involved in the short- and long-term regulation of food intake and energy balance. PYY, synthesized mainly by endocrine cells of the terminal ileum and colon, is released into the systemic circulation in response to a meal and participates in signalling the end of the meal at the hypothalamus. PYY exerts its pro-satiety actions possibly through an Y2 receptor-mediated mechanism. Ghrelin, secreted predominantly from X/A-like endocrine cells of the oxyntic glands of the stomach, is primarily secreted in the fasting state, with plasma concentrations falling within one hour of a meal. Its role in food intake and energy balance is opposite to that of PYY, as it exerts orexigenic effects through activation of the hypothalamic neuropeptide Y-Y1 (NPY-Y1) pathway. We evaluated the secretion of PYY and ghrelin at diagnosis and during chemotherapy in children with ALL. Ten patients aged 2-7years were included in this perspective study. All patients were treated following the same protocol (HOPDA97)1. A physical examination was performed and blood chemistries were evaluated by standard techniques. Preprandial PYY and active ghrelin levels were determined by specific radioimmunoassays (Linco Research, Inc., USA). Measurements were performed at diagnosis prior to chemotherapy and at several time points prior to each next cycle of chemotherapy for up to 18 months (6–10 measurements per patient). Baseline PYY levels were 213.2±85.3pg/ml, increased significantly to 283.9±72.9pg/ml after the induction and consolidation phase of chemotherapy, and returned progressively to pre-treatment levels at the 6th cycle of the maintenance phase. Baseline active ghrelin concentrations at diagnosis were low (32.6±8.6pg/ml), fluctuated throughout the study period and stabilized at significantly higher levels (57.4±31.6pg/ml) after the 8th cycle of maintenance phase of chemotherapy. These data suggest that in children with ALL and anorexia-cachexia the levels of PYY decrease with time, as the leukemic burden is eliminated. In contrast, active ghrelin levels are relatively low at diagnosis, remain low during the early cycles of chemotherapy, but normalize with the elimination of the leukemic burden, paralleling the body weight gain trajectory.

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